Moral of the Story: Don't Cause Gratuitous Pain

I have not been blogging much for several years because my other academic/scholarly activities have taken precedence. But now that I'm a PGY-26, I have accumulated in my mind a bevy of anecdotes that serve as lessons or stories with morals for me, and I'm going to start documenting these here as they occur to me.

When I was a 3rd year medical student on a surgical rotation in 1997 at Ohio State University, rotating at Grant Community Hospital, I was in the surgical intensive care unit (SICU) with a very good resident. A Swan-Ganz catheter was being placed for hemodynamic monitoring in an intubated and partially sedated man. I was eager to witness this procedure. It was a left subclavian insertion site, with a Cordis. The patient writhed in pain with each landmark-guided needle pass. There was no time urgency - for the patient anyway, it was an elective procedure, though the doctors were very busy - and I thought: "there is no need to rush this procedure, why don't we sedate him or give more local anesthesia?"

This experience - I recall it vividly as though it were yesterday - has been burned in my brain as an indelible stamp with the moral: don't cause gratuitous pain.

Bayesian Implications for Factitious Disorder

The next time you encounter a patient with an odd constellation of rare or poorly defined diseases (POTS and MCAS is a common duo), especially if a psychogenic one is on the list (e.g., PNES - not, I presume, intended to be sounded out, as it was proposed as a less offensive alternative to pseudoseizures), do yourself a favor and read one of Mark Feldman's excellent books on factitious disorder, such as the most recent, Dying to Be Ill.

These patients are wellsprings of iatrogenesis, but it is a special variety because the patients actively deceive physicians into unwittingly fostering complications through well-intentioned attempts to diagnose and treat disease. Several biases in medical decision making are exploited by patients with factitious disorder (and its close sibling, malingering, where the reward for the sick role is external - e.g., relief from work, military service or thwarting criminal justice proceedings - rather than internal), and I address some of them in this post.

Numeracy in Medicine: Clinical Wagers to Estimate Probability in Diagnosis

As has become my custom, I offered a wager on rounds the other day. An nonagenarian had gastrointestinal hemorrhage. He presented with syncope and gross (red) blood per rectum. History was significant for Apixaban for atrial fibrillation, and NSAID use. My questions to the team were: what are the possible etiologies of the bleeding; and which among are most likely? After the diagnostic possibilities were enumerated, I offered my wager: a $10 stake that it is peptic ulcer disease (PUD) at 4:1 odds. If the patient has PUD, a taker of my wager owes me $10. If the patient does not have PUD, I owe the taker the $10 stake multiplied by the odds: $40.

There are several pedagogical and practical reasons I engage my team in these games, most of them pedagogical. First, making a wager about clinical outcomes gives you skin in the game. It is remarkable how, when I assign a stake and odds, the interest level goes up and my would-be wager-takers become carefully attuned to the differential diagnosis and other pieces of data that until then had been glossed over or wholly neglected. Recently, when making a wager about results of a pending echocardiogram, the resident did a much deeper chart dive than had previously been done and found a remote echo which bore on the probabilities for the current wager. I had to reassign the odds in light of this new information. Related to this deeper search for available information about the case, there can be a search for information about the diseases under consideration. It would be folly to try to make a bet about the probability of a disease that you understand incompletely, or not at all. Skin in the game will likely lead you to www.uptodate.com where you can ascertain knowledge about the considered diseases to apply it to the wager.

Cheating in Medical School? A Personal Tale in the Wake of the Dartmouth Scandal

A recent NYT article about cheating at Dartmouth reminded me of some hermetic knowledge of cheating in medical school that I have kept mostly secret for almost a quarter century. Without commenting on the Dartmouth case, I will relate this tale to demonstrate that cheating in medical school is real, and my experience is the opposite that of Dartmouth - administrators turned a blind eye to cheating, denying its existence until confronted by direct evidence of it.

In 1996, the "final exam" after an 8-week internal medicine rotation was a so-called "shelf board" exam, which I have always understood as meaning a copy of some prior year's board examination, or a preparation test for it. In medical school in late August 1996, I had the top score on this examination during the first "rotation" of 8 blocks that we did during the third year. I was pleased by this and considered it vindication of my method of not "studying to the test" but instead reading Harrison's Principles of Internal Medicine (13th edition) cover to cover during the second and third years of medical school. I later noted that the top score crept up as the year went on, and I was bemused. Were others reading Harrison's Principles of Internal Medicine? Doubtful. There were rumors of a "question bank" that previous takers of the exam compiled as the year went on, and shared with one another. If the "shelf exam" was only changed each year this would make sense. Alternatively, the kids were just getting smarter as the year progressed.

Applying Applied Physiology to COVID: Silent Hypoxia and The Work of Breathing

Enough time has passed and enough clinical experience with the behavior of COVID gained that we can now apply some applied physiology to our understanding of this aweful illness.  I don't have the answers any more than the next person, but I do know that whatever the behavior of COIVD, it can be viewed through the lens of what we do know about applied lung physiology, and some inferences can be made.  This post will be about that physiology and those inferences, using the frameworks in these lectures about applied physiology.

One of the striking early observations about patients presenting with COVID was their apparent lack of distress despite very low oxygen saturations.  This was termed "silent hypoxia" at some point, and I leave it to internet sleuths to trace its origins.  It led to a policy of early intubation of some COVID patients:

“Never in my life have I had to ask a patient to get off the telephone because it was time to put in a breathing tube,” said Dr. Richard Levitan, who recently spent 10 days at Bellevue Hospital Center in Manhattan.

There are two simple explanations for the observed phenomenon of silent hypoxia: first is that hypoxia is not nearly as potent a stimulus of respiration as is hypercarbia, as I took great pains to explain in the Applied Physiology lectures, using the example of shallow water breath hold divers who do not pre-oxygenate and emerge with sats on the order of 50%, the same as climbers on Mt Everest.  (See also this post on the boy in the wheel well, unpressurized, from California to Hawaii.)  I thank Matt Wong (@EM_phile on Twitter) for pointing me to this video which provides a striking illustration of lack of dyspnea with sudden and severe hypoxemia.  This video is compulsory viewing:

Dyspnea is driven far more by ventilation demands and the work of breathing than it is by hypoxia alone.  This is underrecognized.  I wager this stems in part from the fact that in most diseases that cause hypoxia, there is significantly elevated work of breathing because of parenchymal disease/infiltration (elastic loads) and airway secretions (resistive loads), combined with minute ventilation loads from high CO2 production, dead space ventilation (Vd/Vt) and metabolic acidosis.  If COVID does not have all of those loads, patients may not experience substantial subjective dyspnea despite low oxygen.

Are the "Vent Protocols" causing harm in COVID?

Here is a response to Deborah Mayo's excellent blog post posing this question.  I encourage you to first read her post.  Here, I explicate my view of the problems that are raised in that post.  I don't have time for a lot of hot links and stuff, so post your specific comments below.

There is a lot correct here, and @learnfromerror has done a far better job of summarizing it than I could ever explain a normal distribution. But there is a lot missing, because the commentators have not gotten to the crux, and have made slogans for their points that are distracting and misguided if not totallly incorrect.

First, and this is very very important, is that *there are NO protocols for intubation* as the NYC ER doctor suggests. I talk about that on my other blog a lot. ARDS trials enroll patients who are *already intubated* and the criteria for that intubation are absent from the study protocols. It is assumed in an ARDS study that if you are intubated, you were appropriately intubated. Therefore, there is no “problem with the protocols” for ventilators, there is a glaring and longstanding problem with the criteria (or the absence of criteria) for intubating patients. Is it blood gas values, or vital signs, or physical examination signs, or subjective distress or some combination? There is ZERO standardization in this area. COVID has brought this underappreciated problem to the fore.

Why is this just coming out now? Ah, that’s another crux of the problem and a reason that COVID has become a perfect storm for ventilator management. Usually, if you intubate a little old lady with influenza, even if you do it for shaky reasons, she can be extubated (tube removed) in a couple of days or a week with little harm done (or with a level of harm that we take for granted, probably mistakenly). Not so with COVID. The natural history of the disease has 2 important features that make the decision to intubate likely to culminate in a massive therapeutic misadventure: 1.) the duration of the illness is protracted, two to perhaps as long as four weeks; and 2.) the level of sedation needed to counteract the massive air hunger these patients have, for the duration they need it, is through the roof.  This problem is compounded by the mandate to use small tidal volumes which are poorly tolerated in the face of massive air hunger. So, 2 weeks after intubation, they are veritable zombies, cannot be weaned from sedatives (a prerequisite from being weaned from the ventilator), and are stuck on the vent, assuming that before this stage other complications have not set in and/or death ensued.

Another facet of the perfect storm, which I think is also the Rosetta Stone, and a key to untangling this giant mess we find ourselves in, is that this normal lung compliance that people are talking about is *the reason why* there is this so-called “silent hypoxemia” of the type mentioned by the ER doc in Mayo’s post. Failure to recognize this connection betrays a common misunderstanding of respiratory physiology (my attempt to disabuse people of these errors can be found here: https://pulmccm.org/ards-review/great-lecture-applied-respiratory-physiology/). Dyspnea is not driven by hypoxemia as much as it is by hypercarbia, which can be compensated for by hyperventilation which these patients are doing! To a person who has a firm grasp on applied respiratory physiology, this is no surprise – the patients have compliant lungs, so they don’t have workload imbalance and can sustain ventilation in the face of significant hypoxemia (which is a MINOR driver of dyspnea) very well. In sum, I am not surprised by these clinical presentations, nor am I surprised that this quagmire has allowed problems with the understanding of applied respiratory physiology to surface.

This disease is very difficult for these and many other reasons. When the choice is let a hypoxemic person who is defending her CO2 - like the little old lady the ER doc talks about - ride it out (which she can probably do for a very long time, see my tweets about sustaining very high Ve indefinitely [50% of the 15-second MVV]), versus intubating her for a marginal gain in gas exchange accompanied by a massive cost in sedation and paralysis, the choice is clear, let them ride it out, don't incur that cost.

The problem is not with the “vent protocols” the problem lies in a widespread lack of understanding of applied respiratory physiology which leads to questionable calls regarding intubation which are usually, in non-pandemic times, lost in the signal and noise of the fray. Not so with COVID – premature or unnecessary intubations precipitate a cascade of status iatrogenicus.

"I'm Not Comfortable With"....Analyzing Decisions Involving Risk

A woman with upper gastrointestinal bleeding is admitted to the ICU with significant hemoglobin drop from baseline several months before.  The INR was >10 on admission, presumably reflecting sphlanchnic hypoperfusion during the bleeding episode (decreasing clearance or increasing effect of warfarin) in addition to consumption of clotting factors during bleeding.  The INR is reversed with vitamin K, and an EGD is performed showing a nonbleeding vessel which was clipped.  The following day, the patient is up and walking around and eating a full liquid diet with no further evidence of bleeding.  MAPs are in the mid to low 60s, and she is "called out" for a transfer to the regular medical ward.  The resident is reportedly "not comfortable with" having the patient on the floor with the low mean arterial pressures.  How best to analyze the situation?

(I will only briefly note that the expression of discomfort describes an emotional reaction that may or may not be concordant with a logical and factual analysis of the situation at hand.  In this case I suspect it has something to do with the availability heuristic, where dramatic events [gushing blood] are estimated to have higher probabilities than they warrant.)

The discomfort seems to stem from a concern that the patient will deteriorate on the regular medical ward and require interventions that are not available there, prompting readmission to the ICU and incurring the risk of a missed opportunity to provide necessary care during any delays in executing the transfer.  Factors that may raise that concern are marginal hemoglobin values (7-8) especially considering a baseline of almost twice that several months before, the size of the GIB and the resulting hemodynamic instability, the marginal MAPs at the time of transfer.  Mitigating factors are the absence of ongoing bleeding, the inference that any marginal MAPs must be from a residual volume deficit (she does not have coincident sepsis), that the vessel was successfully clipped, and the patient is up and walking about in spite of the measured MAPs.  But how are we to integrate this into an estimate of the risk that may be incurred from transfer?

The Bermuda Triangle of Guidewires: Do They Just Fly Away Never to Be Seen Again?

In last week's NEJM, author Matt Bivens reports an extraordinary experience: while inserting a venous catheter, he let go of the guidewire and moments later looked and saw it migrating into the patient's jugular vein, on its own.  He grabbed it as it was running away, just before it escaped from him.  While I can imagine, as he did, how it may have happened, it is an exceptional claim.  Some aspect of the venous circulation or respiratory motion must have been pulling the wire downstream into the patient, if this story is true.  I say "if" because it is truly extraordinary.  Not only must the venous circulatory flow have been "grabbing" the wire, carrying it downstream, it had to do so with enough force to overcome the friction of the wire as it traversed the tissues of the neck.  (Not mentioned is the size of the patient's neck or whether this happened pre- or post-dilation, or whether the patient was in Trendelenberg - if so the catheter had to be pulled up hill!)

I have never seen or felt a guidewire move in such a way, over 20 years and thousands of lines.  However, I did turn my back on an intern circa 2000 and that intern pushed and/or flushed the guidewire into the patient.  So I was interested in the 4 references in the article purporting to show that guidewires have wings or feet or that the venous circulation can pull them and overcome the tissue resistance and mass of the wire.  Here is a summary:

The Truth Doesn't Always Need A Test: Thresholds for Medical Decisions

Jason Carr, MD didn't need a test to know what this is

Kassirer (and Pauker) got the idea for the Threshold Approach to Medical Decisions in part (as he tells it in his memoir Unanticipated Outcomes) because he had observed a pattern of irrational behavior among nephrologists (he was one) in the 1960s.  Evaluating a patient with nephrotic syndrome and knowing the diagnosis was very likely to be membranous glomerulonephritis, most nephrologists still insisted on a biopsy prior to starting corticosteroids.  Pauker and Kassirer realized that we never get to 100% certainty in medicine and that tests only modify the pre-test probability of disease.  They reasoned that there ought to be a threshold of pre-test probability of disease that is high enough to justify treatment without testing.  That is, sometimes, the pre-test probability of disease is so high as that it obviates testing, and we can just skip to treatment and avoid risky and invasive testing like a kidney biopsy.  Only if the disease fails to respond to therapy (thereby reducing the clinical pre-test probability below the treatment threshold) should we resort to the biopsy.

Almost 40 years after the publication of their article, we still are not consistently following the axioms of the threshold approach.  Here are several recent examples:

A 20-something black woman presents with cough, weight loss, massive hilar and mediastinal lymphadenopathy and interstitial parenchymal changes.  She is scheduled for a bronchoscopy and EBUS to confirm the diagnosis of sarcoidosis prior to initiating corticosteroids.

The Test is Not the Truth: One Week in the Lonely Life of a Bayesian Clinician

DAH from GPA or CPE/ESRD?

If there is one thing you should remember about clinical decision making it is this:  the test is not the truth.  A diagnostic test raises or decreases the prior or pre-test probability (PTP) of the disease under consideration.  The amount of increase or decrease in probability with a positive or negative test depends on the starting probability and the likelihood ratio of the test.  (LR+ = sensitivity/1-specificity; LR- = 1-sensitivity/specificity).  If we don't attend to the PTP of disease, serious diagnostic errors and therapeutic misadventures may result.  This is especially true when a low PTP disease is diagnosed on the basis of a test with poor sensitivity and specificity (and a LR not much greater than 1 or 2 or even 4 or 5).  Several examples of this came up a while back.

A woman presented with thunderclap headache and had recurrent seizures during initial evaluation.  A differential diagnosis was formulated and it included PRES (posterior reversible encephalopathy syndrome) with a PTP of about 20%.  Subarachnoid hemorrhage was excluded with CT and LP and the PTP of PRES rose to about 40% (since it occupied some of the probability space previously occupied by SAH once the latter was excluded.)  The subsequent MRI images were consistent with PRES.  Nonetheless, a vascular MRI was ordered to "exclude the possibility of cerebral vasculitis".  The problems are twofold.  First, the probability of PRES is now on the order of 70% if the sensitivity and specificity of MRI are on the order of 80%, and it is 85% if sensitivity and specificity are each 90%.  (Go ahead and plug some numbers into the calculator on the sidebar of the blog.)  This probability meets or exceeds the probability threshold to both consider the diagnosis made, and to take action based on it.  In this case inaction and supportive care are indicated.  Even if a vascular MRI were consistent with cerebral vasculitis, which has a PTP an order of magnitude or more less than PRES, the diagnosis is still PRES.  The truth is not in the test, the truth is in the rationally considered diagnostic process of which the test is one part.

Pitfalls of Protocols: Pushing the Limits of Extubation

A recent post described extubating an asthmatic patient with very bad weaning parameters, and I promised to provide a followup telling whether he "flew" or not.

He flew.

It was a nail-biting experience and for the first hour it was unclear if he was going to make it.  His respiratory rate settled down into the teens which was reassuring, but he did not gain lucidity for quite a while and was intermittently midly "combative" and uncooperative.  He was on HFNC with oxygen saturations in the high 80s and low 90s, and he remained tachycardic and was wheezing.  His wife and the nurse were continuously in the room reassuring him, as were several doctors during the first hour or two.  During the course of several hours, he was able to be weaned to simple face mask and then nasal cannula and the next day he was discharged from the ICU.

If we had followed some sort of "weaning protocol" with blind faith, I don't know how long it would have been before he would have "passed" the protocol's tests and been extubated.  At some point, somebody would have said, "Hey, we better stray here, or we'll never get him extubated."

Limits of the Possible: Clinical Reasoning of a Harrowing Extubation

"The only way of discovering the limits of the possible is to venture a little way past them into the impossible."  -  Clark's Second Law

In prior posts here and on the Medical Evidence Blog (here, here, here, and here), I have outlined my position that the only way you can really know if a patient can breathe on their own is to let them try - a "trial of extubation".  Prediction equations get you published, but their signal to noise ratio is often poor and ignored, to patients' peril.  Indeed the reason I'm obsessed with extubation is because I think being intubated unnecessarily is one of the worst things a patient can endure, and the best thing I can do as an intensivist is identify the earliest moment when a patient can breathe on his own and extubate him.

I faced a very harrowing extubation decision recently, and I admitted to the medical students that it was the most nail-biting of my career.  But I think analyzing it, both before and after the fact can be very instructive.

Speed Matters: Landmark Guided Left Subclavian Vein Central Venous Catheter Insertion & the "Deep Spot"

Recently, I got permission from a patient to video a subclavian line insertion.  This patient was absolutely terrified of any line insertion as he had had many in the past and a lot of them had been traumatic, prolonged, and painful.  I offered a bedside subclavian as an alternative to a PICC line or a right internal jugular in Interventional Radiology, promising that the entire procedure could be done in under 10 minutes.  It took just over 2 minutes, excluding prepping, draping, locally anesthetizing, and suturing.  These aspects would have added about another 3-4 minutes to the task.  Before the video started, I had infiltrated the area generously with 2% lidocaine, after prepping and draping in the usual careful fashion.

Before you watch the video, I should describe the essence of subclavian landmarking and several mandates of the procedure.  The key anatomical landmark is a spot seen in the photo accompanying this post that I call "the deep spot."  This is a spot along the inferior border of the clavicle, about 4 inches from the suprasternal notch (SSN).  It is important because it is the spot where soft tissue adjacent to the inferior border of the clavicle can be depressed the deepest, allowing the needle the easiest access to the subclavian region while being inserted "FLAT, FLAT, FLAT, FLAT, FLAT" under the clavicle with respect to the ground, i.e., parallel to the ground.  Entering the subclavicular region in this spot and remaining flat/parallel to the ground are keys to both success and avoidance of the oh-so-feared (but rare!) pneumothorax.

This spot can be found by making the middle finger and the thumb of the non-dominant hand into a comfortable "C" shape as seen in the photo.  The middle finger and thumb will be parallel to each other when in the "C" shape and will be about 4-5 inches apart depending on your fingers and the patient's anatomy.  With the middle finger in the SSN, the thumb finds the spot along the inferior border of the clavicle where the skin can be depressed the deepest.  If you're too medial, you will be atop ribs and "too high not deep enough" and if you're too lateral from the SSN, you will start climbing up the humeral head and deltoid and be "too high, not deep enough".  If you are too close to the clavicle or atop it, you will not be in the "deep spot" (it is a finger breadth or so inferior) and if you go too inferior from the clavicle, you will climb atop the pectoralis/breast and not be in the deepest spot.  Find the "deep spot"!  Again, the point (no pun intended) is to find the spot where the tissues near the clavicle can be depressed the deepest to facilitate the insertion of the needle under the clavicle and parallel to the ground.  This cannot be overemphasized, and you can feel for that spot on yourself or a willing companion for practice.

Once this spot is located, you anesthetize and then use the needle to confidently identify the clavicle and by advancing the needle towards the SSN, you can press down with your thumb on the needle (even the part under the skin) to depress it so that when advanced, it is parallel to the ground towards the SSN and it goes easily under the clavicle.  You should never "dive" to try to get under the clavicle, or use the clavicle as a fulcrum, bending the needle downward.  Watch the video carefully to see how I'm using several tactile inputs to determine where the clavicle is as I guide the needle under it.  You will see that the first several "pokes" or short advancements of the needle hit the clavicle (it happens fast, watch carefully!) which is a very important tactile confirmation of where you are, and then I push the inserted needle down with the left thumb to allow the advancement to proceed below the clavicle.

As seen in the video, the SCV is often entered when the needle is maximally inserted ("hubbed") with the skin invaginating, or upon withdrawal.  Notice too in the video that the flash was subtle at first and too rapid a withdrawal might have missed it.  Also in the video, the flash was highly positional, and the exact optimal position had to be found by iterative advancement and withdrawal and then maintained by carefully pinching the hub of the needle with the hand referenced to the patient's chest to allow the wire to be fed without inadvertent and unrecognized migration of the needle out of the vessel.

The voice overlay of the video gives several other useful tips and I hope you enjoy watching it.  The SCV central line is one of the final remaining procedures where use of ultrasound guidance (USG) confers minimal, if any benefit, and USG markedly prolongs this (and all) procedures.  Over my career during the past 20 years, I estimate I have done 500 or more SCV catheters all guided by landmark, most in critically ill patients.  I had *one* pneumothorax (PTX), in 2011 in a patient with severe COPD.  (I also supervised a resident once where there was a PTX, and to this day I don't understand how it happened.)  In properly trained hands, this procedure is incredibly safe, is the preferred location for a central venous catheter in terms of patient comfort, and infection and thrombosis risks, can be performed with a very high success rate using landmarks alone, and can be done very speedily.  Speed is the final frontier: Safety, Success, Speed.

Here is the NEJM.org video, for comparison:  https://www.youtube.com/watch?v=braNvVl8-QU

And here is a Right Internal Jugular HD Catheter insertion using landmarks by The Phlegmfighter (yours truly).

Activated Charcoal and Beta Blocker Overdose: Clinical Decision Making and the Risks of Dichotomization

This very nice case report in the current issue of the Annals of the ATS is an opportunity to discuss rational clinical decision making.  The authors did almost everything that I would have done in this case and it is a lovely discussion of this toxidrome and its treatment.  There is just one simple and apparently inconsequential decision that I disagree with and I intend to use it as a springboard to discuss rational clinical decision making.

The young woman had a multidrug overdose including metoprolol succinate, extended release.  She presented in shock.  The authors state "Gastrointestinal decontamination was not performed because her ingestion was suspected to have occurred several hours before admission" [emphasis mine].  I have already in an early post on this blog, discussed the inadequacy of the existing data and experimental models on the timing of charcoal administration, which interested readers can read about here.

Studies of the timing of Activated Charcoal (AC) administration use normal volunteers taking therapeutic doses of drugs (for ethical reasons).  We have inadequate data on the speed of absorption of drugs in people who are shocked or who take very large doses of drugs, or extended release drugs.  To dichotomize the efficacy of AC by a bright line of 30 or 60 or even 120 minutes is a gross oversimplification of reality that belies overconfidence in the existing data and experimental models.  This patient took a large dose of a sustained release medication and at some point became shocked presumably causing splanchnic vasoconstriction.  She also took Tramadol and other medications which may slow gut motility via anticholinergic or other effects.  And there may be other unknowns - other medications she took that slowed absorption of the sustained release metoprolol that we don't even know about.

Root Cause Analysis: Dig Deeper, or the Weed Will Keep Growing Back

In a recent JAMA Performance Improvement piece, the authors describe the case of a man who presented to the emergency department with dizziness.  He was sedated for an MRI, his history of OSA (obstructive sleep apnea) may have been glossed over, and he arrested in the radiology department.  The subsequent "root cause analysis" traced the untoward outcome to a failure to recognize the OSA and the adverse effects that may follow sedation of a patient with this diagnosis.

The problem with this "root cause analysis" is that it assumed that the MRI, requested by a neurologist on-call, via telephone, was necessary.  It was not.  The root cause analysis got it wrong because it did not trace the roots to their deepest source:  glossing over the patient's chief complaint and considering it and its evaluation carefully and rationally.  Stroke is an uncommon cause of dizziness and the MRI was probably not indicated, especially in light of the other information provided in the case.

Here is the letter that I sent to JAMA which was not accepted/published.  It is a case of the distinction between rationality and intelligence.  Very intelligent people traced the "cause" or the "root" of the complication to a missed piece of information (OSA) and corollary ideas (he may have complications from sedation), but they failed to consider underlying assumptions:  namely that the MRI was necessary or would yield net benefit in the first place. 

Medicine is best played like chess, not like checkers.  "Intelligent people have superior performance when you tell them what to do."  A failure of a "root cause analysis" such as this will foment the regrowth of the weed.

Here is the letter:

I enjoyed the Performance Improvement case describing oversedation of a patient with obstructive sleep apnea¹.  I posit that the most proximate possible root cause of the complications described was ordering an MRI with low clinical yield², without pre-specifying what abnormality was being sought as well as its probability, and without delineating, a priori, how any resulting findings would change management³.  Presumably, the neurology consultant was looking for stroke.  What was its pre-test probability in a patient with dizziness?  Would management have changed if stroke were detected with imaging?  Were there contraindications to therapies for stroke?  Was the patient already receiving the indicated therapy for stroke?  What is the probability of a false positive finding (i.e., one that doesn’t explain the patients’ symptoms; an “incidentaloma”), and how might that finding lead to interventions which may yield net harm if stroke is not present?  What was the response to meclizine and odansetron, and how did this incremental information alter the prior probability of stroke?  Because decisions necessarily precede actions, they must always be considered as possible proximate causes of downstream complications.  Even if the other errors identified in the reported root cause analysis can be avoided in the future, injudicious testing may lead to other complications, including cascades of additional potentially harmful testing and intervention unguided by careful, rational, clinical decision making.

1. Blay E, Jr, Barnard C, et al. Oversedation of a patient with obstructive sleep apnea prior to imaging. JAMA 2018;319(5):495-96. doi: 10.1001/jama.2017.22004

2. Fakhran S, Alhilali L, Branstetter BFt. Yield of CT angiography and contrast-enhanced MR imaging in patients with dizziness. AJNR American journal of neuroradiology 2013;34(5):1077-81. doi: 10.3174/ajnr.A3325 [published Online First: 2012/10/27]

3. Pauker SG, Kassirer JP. The threshold approach to clinical decision making. The New England journal of medicine 1980;302(20):1109-17. doi: 10.1056/nejm198005153022003 [published Online First: 1980/05/15]

Confusion, Diaphoresis, and Hyperventilation Aboard a Private Airplane

This was intended to be a case report but the amount of work required to publish a case report is just too great to justify it.  The publishing landscape has been flooded with an attendant raft of predatory journals, so one must be very careful.

This will be an online interactive case report.  I will tweet this post, asking for comments and diagnoses in the comments below (preferable to twitter comments) and update with the answer and a discussion in 1-2 weeks.

A 68 year-old otherwise healthy male passenger was flying with his friend, a pilot, in a private plane from California to Montana for a fishing trip.  Within an hour after takeoff, he became confused and diaphoretic and was hyperventilating, then he lost consciousness for approximately 20 minutes.  The pilot applied supplemental oxygen and checked his passenger's arterial oxygenation via oximetry, finding it to be 95%.  The flight was diverted for a medical emergency.  During descent and landing, the passenger regained consciousness but remained confused.  In the emergency department of a nearby hospital, he had normal vital signs, and had a non-focal neurological examination, but remained confused.  Representative images from CTA of the chest are shown below (click on the images to expand).  A head CT was normal excepting for some age related atrophy.  What is the diagnosis?

Sunk Kidney Bias: A Lethal Form of Sunk Cost Bias

Hal Arkes

The heuristics and biases program of Kahneman and Tversky, once an obscure niche of cognitive psychology, became recognized among lay persons with Kahneman's Nobel prize in economics in 2002.  The popularity of the program surged with Kahneman's book Thinking Fast and Slow several years ago and several among the scores of related books about behavioral economics became best-sellers.  This year, Richard Thaler was the Nobel laureate in economics for his work in behavioral economics.   I became aware of heuristics and biases just before Kahneman's Nobel and started looking for them in medicine in 2003.  We (Aberegg, Haponik, and Terry, Chest, 2005) indeed found evidence for omission bias, and have discovered other biases along the way, some which are very intriguing but we aren't even sure what to name them (Aberegg, Arkes, and Terry, Medical Decision Making, 2006).  My point here is that these biases are useful but difficult to identify as patterns systematically operating within medical practice in predictable ways - they pop up here and there only to recede and reappear years later, if they are recognized at all.

Then there are biases about the biases.  Highly cited expositions of biases in clinical care, such as those of the insightful emergency physician Pat Croskerry (Academic Medicine, 2003), among many others) very often surmise the presence of biases in clinical care, without the kind of empirical evidence that established the biases in the first place.  Sometimes, new and probably useful biases are proposed (such as "search satisfycing"), without any empirical evidence, at all in any domain, for their existence.  They are merely postulates.  (Granted, empirical evidence is very difficult to generate, this the reason I don't do this kind of research anymore.)  Finally, the descriptions of the biases applied to medicine are often strained, or just plain wrong.  My favorite is the bastardization of "anchoring and adjustment" into a description of any time a physician seizes upon a diagnosis and discounts disconfirming evidence or fails to consider alternatives.  This is not anchoring and adjustment.  Anchoring refers to a numerical anchor, and failure to adjust away from it when providing numerical estimates.  Here is a summary of the original descriptions, from the wikipedia entry on anchoring and adjustment:

Applied Respiratory Physiology Vlog. Parts 1,2,3,4: Respiratory Failure Explained as Workload Imbalance

The following embedded videos are parts 1-4 of a 5 part talk I've been giving and refining on Applied Respiratory Physiology for about 10 years now.  (It is split into 5 parts because of youtube size limitations and for digestible 10-15 minute segments.)  The principles herein derive from many sources, but special credit must go to Nunn's Textbook of Applied Respiratory Physiology and The University of Chicago critical care text edited by Hall, Schmidt, and Wood.  For the majority of the ideas and applied principles herein, I have never seen them discussed in any lecture in 20 years of attending pulmonary conferences, didactics, etc.  My interest in applied physiology and Nunn's textbook indeed originated because of my frustration with the esoterica of the basic and advanced physiology that I was taught from medical school through fellowship -  I determined that much or most of it was not applicable at the bedside.  This lecture series, I hope, will be far more clinically applicable, intuitively appealing, memorable, and useful than what has been traditionally taught.  Real life examples highlighting the extremes of human respiratory performance should, I hope, make this a memorable lecture seeries.  I welcome comments and criticisms below.  Enjoy!

DIPSHIS: Diprivan Induced Pseudo-Shock & Hypoxic Illness Syndrome

This would be a very informative case report (and it's true and unexaggerated), but I anticipate staunch editorial resistance (even sans puns), so I'll describe it here and have some fun with it.

Background:  The author has anecdotally observed for many years that so-called "septic shock" follows rather than precedes intubation and sedation.  This raises the possibility that some proportion of what we call septic (or other) shock is iatrogenic and induced by sedative agents rather than progression of the underlying disease process.

Methods:  Use of a case report as a counterfactual to the common presumption that shock occurring after intubation and sedation is consequent to the underlying disease process rather than associated medical interventions.

Results:  A 20-something man was admitted with pharyngitis, multilobar pneumonia (presumed bacterial) and pneumomediastinum (presumed from coughing).  He met criteria for sepsis with RR=40, HR=120, T=39, BP 130/70.  He was treated with antibiotics and supportive care but remained markedly tachypneic with rapid shallow respirations, despite absence of subjective respiratory distress.  A dialectic between a trainee and the attending sought to predict whether he was "tiring out" and/or "going into ARDS", but yielded equipoise/a stalemate.  A decision was made to intubate the patient and re-evaluate the following day.  After intubation, he required high doses of propofol (Diprivan) for severe agitation, and soon had a wide pulse pressure hypotension, which led to administration of several liters of fluids and initiation of a noradrenaline infusion overnight.  He was said to have "gone into shock" and "progressed to ARDS", as his oxygen requirements doubled to 80% from 40% and PEEP had been increased from 8 to 16.  The next morning, out of concern that "shock" and "ARDS" were iatrogenic complications given considerations of temporality to other interventions, sedation and vasopressors were abruptly discontinued, diuresis of 2 liters achieved, and the patient was successfully extubated and discharged from the ICU a day later.

Conclusions:  This case provides anecdotal "proof of concept" for the counterfactual that is often unseen:  Patients "go into shock" and "progress to ARDS" not in spite of treatment, but because of it.  The author terms this syndrome, in the context of Diprivan (propofol) in the ICU setting, "DIPSHIS".  The incidence of DIPSHIS is unknown and many be underestimated because of difficulty in detection fostered by cultural biases in the care of critically ill medical patients.  Anesthesiologists have long recognized DIPSHIS but have not needed to name it, because they do not label as "shock" anesthetic-induced hypotension in the operating theater - they just give some ephedrine until the patient recovers.  DIPSHIS has implications for the epidemiological and therapeutic study of "septic shock" as well as for hospital coding and billing.

The Number Needed Not To Treat To Harm (NNNTTTH): A Heuristic for Evaluating Trade-offs in Medical Decisions

A frequent conundrum of decision making that arises in medicine is when there is a generally indicated therapy, say, anticoagulation for atrial fibrillation, that poses unique risks in a particular patient.  CHADS2 and HAS-BLED scores are calculated, but don't quiet the hemming and hawing or quell the hand-wringing.  What is usually a simple dichotomous decision is now one laden with probabilities, risks and benefits, and compromise between competing objectives.  (See:  The Therapeutic Paradox:  What's Right for the Population May Not Be Right for the Patient.)  In order to restore nuance to the decision, we need to try to estimate the numerical values of the risks and benefits to determine if the net utility of anticoagulation is positive or negative, something the aforementioned calculators are intended to do in a semi-quantitative way.  But what if you opine that your patient has a specially enhanced risk of side effects and you're worried about falls or bleeding but ambivalent because of a concurrent fear of denying him of the benefit of stroke prophylaxis?  What if you think that he would have never been included in a trial of stroke prophylaxis and the results of those trials may have limited generalizability to him?  What if you think he has only a year to live?

The number needed not to treat to harm (NNNTTTH) is the number of patients whom you have to not treat with something beneficial in order to cause one harm from your omission.  It is numerically equivalent to the number needed to treat (NNT), but it reframes the decision from action to omission and from benefit to harm.  Ignoring bleeding altogether (because making relative utilities for bleeding and stroke is a fraught endeavor), you could ask yourself "how many patients can I withhold stroke prophylaxis from for one year before I statistically cause (or allow to happen, if you are prone to omission bias) a stroke?"  For most patients, withholding stroke prophylaxis has a NNNTTTH of about 25-30 per year (check the corresponding NNT from CHADS2 for a more "precise" estimate).  Reframing the question into "how much am I asking the patient to pay, in terms of statistical likelihood of stroke, to avoid anticoagulation and the particular side effects that cause me concern in his case?" can often provide some reassurance for the clinician and the patient alike.

Screening in Disguise: You Can't "Unknow" that Troponin, But You Can Dismiss It After Careful Thought

During MICU rounds last month, there were a lot of troponins ordered, and most of them should not have been.  Invariably when abnormal troponin values are reported on rounds, there is no mention of whether the patient had anginal chest pain, whether there were ischemic EKG changes, or whether this information was sought at the time the troponin was drawn.  This is because troponins are being used as a screening test, rather than as a diagnostic test.  "Not so!" exclaims the resident, eager to convince me that he has not engaged in the kind of mindless testing he knows I loathe.  I am told that because the first troponin was mildly elevated in a little old lady with cirrhosis, overdose, right heart failure and urinary tract infection, that we need to follow it to see where it "peaks".

The Enemy of Good is Better: Maximizing versus Satisficing in Clinical Medicine

Herbert Simon, Nobel Laureate

Recently I was called to admit a little old lady with a digoxin overdose who had symptomatic bradycardia.  She was in her 70s, had Alzheimer's disease (AD) and a medication list that would not print on one page.  I immediately thought, what benefit does digoxin have that justifies even the occasional admission for toxicity?  That's a good question in its own right, but consider a partial list of her other medications:

1. pantoprazole
2. lisinopril
3. gabapentin
4. raloxifene
5. estradiol
6. donepezil
7. labetolol
8. furosemide
9. glipizide
10. fenofibrate
11. memantine
12. sitagliptin
13. spironolactone
14. amlodipine
15. alprazolam
16. aspirin

One certainly must wonder what goals her providers are trying to achieve with these and indubitably some other medications which aren't listed.  Her husband was frustrated when I told him that many of the medications she is taking are not really doing her any good.  "They why do they have her taking them?" was a question I could not answer, because it doesn't make sense to me either.  Exasperated, he offered a great analogy:  "Suppose you hire me as a contractor to build you a home, and I tell you that you need to build a 14 foot high retaining wall in the back yard, two feet thick, reinforced with rebar and containing 20 yards of concrete.  Would that be responsible unless it were absolutely necessary?  What kind of contractor would recommend something you didn't really need?"

"A physician contractor," came the ready answer in both of our minds, and we simultaneously nodded in understanding.

Medical Decision Making as a "Patient": Pregnancy Leads to A Trip Down The Rabbit Hole - A Personal Story

My wife is pregnant.  Wanting to be a supportive spouse, I attended the first prenatal visit to see one member of her team of midwives.  (Being a "minimalist" I was, like my wife, fond of the idea of not unnecessarily "medicalizing" the [usually] natural act of labor and birth.)  I realized during that first visit that understanding the intricacies of medical decision making can be a double-edged sword when dealing with practitioners, especially outside of one's specialty.  If ignorance is bliss, 'tis folly to be wise, it is said.  I've come to wonder which is better for you when you get entangled in US healthcare, wisdom or bliss.

During the first visit, we were offered, with an air of agnosticism, a referral for genetic counseling +/- non-invasive prenatal testing (NIPT).  "How accurate is it," I naturally inquired, trying to avoid technical terms such as sensitivity and specificity.  "Something like 99%" came the reply.  So we were given the referral.  But I quickly realized that this was a classic problem of base rates.  The likelihood of a chromosomal abnormality is so low given my wife's age, that even extremely high sensitivities and specificities are inadequate to guide our decision - that is, the test is rendered practically useless because of the low base rates in our case.  And this despite the fact that the sensitivities and specificities of prenatal blood testing are inflated by the way they were derived.  But think of the decision we would have faced had we blindly proceeded with testing without this consideration - given the low base rate, the posterior probability of a chromosomal abnormality such as Down's Syndrome given a "positive" test result would be around 33%.  How would we act on this information?  Is that threshold high enough that we would consider an elective abortion (if we were morally disposed towards that as an option)?  Or would we ignore the information and proceed to term?  And if we were not ethically accepting of elective abortion as a possibility, what other remedy would we have that would justify the information from the testing?  Why would we talk about getting prenatal genetic testing before talking about the choices we may have to face after we receive the results?  Why would not a discussion of remedies, specifically abortion, precede consideration of the testing?  How many couples dive into the rabbit hole only to wonder how they got there and how they can get out?  In this case, we decided that ignorance was indeed bliss, and deferred NIPT.

At that same visit, blood was ordered to be drawn.  I had difficulty understanding why you would need to draw blood from a perfectly healthy woman at 12 weeks gestation.  Blood types and anemia and all that I guessed.  But I was particularly caught by the thyroid testing.  Why are we screening an asymptomatic woman for thyroid disease?  Is that justified by the prior probabilities?  It takes only a google search to learn that ACOG (the American College of Obstetrics and Gynecology) and an endocrine society do not recommend universal testing.  But my questioning why we were doing this was off-putting and frankly unanswerable for the midwife - she was just following the usual routine, whatever her supervisors and mentors had told her to do, without understanding....well without understanding any of this Bayesian mumbo jumbo that I was hinting at.  Alas, thyroid testing, like NIPT, was deferred.  But not for long.

The Lost Art of Landmarking: Right Internal Jugular Insertion Video

I have long wanted to post a video of central line insertion using the traditional landmarks method, and recently I was afforded the perfect opportunity.  The patient needed a dialysis catheter.  He had had one inserted a few months ago and it had been a disaster for him.  First, the inserting physician mistakenly installed a Cordis Introducer instead of a dialysis catheter, using ultrasound guidance and causing a good deal of pain by transecting the belly of the sternocleidomastoid (SCM) muscle, then it was rewired to a dialysis catheter that would not flow, then, finally, a working catheter was installed in a new site.  I assured the patient that this go at it would be much easier and he was very interested in having the experience recorded so he could later see it, and others could learn from it.

I previously observed that in the current training atmosphere, trainees are paying no attention to anatomical landmarks, rather they are just poking wherever they see the vein on the ultrasound image, traversing whatever structures lie between the surface and the target, without any care whatever.  It is my belief that the SCM muscle should never be split/transected with a dilator or line unless absolutely necessary.  Thus even if ultrasound is used, the landmarks ought to be identified and respected.

Several points in the video need further explication here.  (Beyond the facts that my nose did not fit under the mask, I did not wear eye protection, and that I failed to lay out the components of the tray beforehand.)

• The importance of properly and confidently identifying the bellies/heads of the SCM cannot be overemphasized.  I will at some point do another video to go through that process specifically in detail.
• I always keep 0.5-1.0 cc of liquid (lidocaine or flush) in the syringe during needle passes.  In my experience, it minimizes clotting in the needle and the risk of passing through the vessel without flash due to clot.
• In contrast to what is suggested in the NEJM video for RIJ CVC insertion, I do not hold the needle at 45 degrees to the floor plane when going after the IJ.  Doing this makes you have to insert the needle much deeper, increasing the risk of pneumothorax.  I prefer an angle of 60-90 degrees.
• In this patient, the IJ was deeper than usual and than I expected, thus I did not hit it with the "seeker" needle.
• When the fingers of my left hand are on the neck, I am not palpating the carotid pulse.  I could care less about the carotid.  I am feeling that medial belly of the SCM as a landmark and ever so gently pushing it to the left to increase exposure of the IJ underneath of it.
• When entering the skin with the large bore needle, I poke to and fro rapidly to keep it from "breaking through" the skin and plunging too deep.
• Notice that each centimeter or so that I enter with the large bore needle, I pause and pull back a bit to see if I get flash in case the vessel is compressed on the forward pass.  In the video, I get flash on the second or third pull back.
• After I get flash, I then lay the needle back to 45 degrees to facilitate guidewire passage
• This patient's skin and subcutaneous tissue was tougher than I expected and I did not make a generous enough stab incision into the subcutaneous tissues to make a tract for the dilator.  Usually I use a regular 7.0 French triple lumen CVC kit dilator first, then the smaller of the two dilators that come with the larger 12 French dialysis catheter.  This is a new all-inclusive kit that we began using which contains only the large dilators.
• The bleep is to protect privacy

Stay tuned for the subclavian vein CVC insertion video next!

[Formal written consent was obtained from this patient to make this video and to publish it for educational purposes.]

Special thanks to Clayton MS4 for filming this and helping with editing.  Other medical students are encouraged to participate in future web and social media initiatives.  I have several in mind.

Doctorin' with Double Effect Part II: The Devil is in the Details

In a prior post, Doctorin' with Double Effect, (a double entendre with Doctrine of Double Effect) I attempted to tease out ethical issues related to the withdrawal of life support and specifically the provision of oxygen in dying patients.  The simplest case is that of a moribund patient who is completely dependent upon life support measures such as mechanical ventilation and vasopressors.  In such a patient, withdrawal of these measures often allows a quick death to ensue.  Provision of oxygen in such a patient will not avert death, but will prolong it, so I think that while oxygen is often reflexly applied to such patients, I can say with some confidence that it should not be.  While it is mostly benign, it generally does not provide comfort and it prolongs the dying process so it is on the net futile or harmful.  I struggle to reconcile my strong pragmatic intuition about this with ethical principles such as the DDE, although I think it is consistent with the notion that I can take away something that restores a natural state to abrogate its associated discomforts or in deference to patient autonomy and a wish to have a "natural death."

But there is a very large grey area.  What about patients in whom death is not imminent?  Consider a patient who has been on the ventilator for a week with dementia and aspiration pneumonia, and who has developed weakness.  He is alert, but not oriented.  When he is extubated, it is expected that he will develop retained secretions, atelectasis, and over several days, obtundation and oxygenation and ventilation failure.  But over several days.  Should oxygen be administered in the hope that he will rally?  Does its deprivation deprive him of a chance of survival that is disproportionate to the removal of the endotracheal tube and the mechanical ventilator in terms of net costs and benefits?

Or, consider the patient who is demented and is admitted with pneumonia from aspiration and who is DNR/DNI and is given supplemental oxygen.  Does escalation of oxygen therapy to a non-rebreather mask from nasal cannula fly in the face of his DNR order?  Does the administration of peripheral vasopressors for hypotension have the same result?  Does DNR/DNI mean Do Not Respond/Do Not Intervene?

Don't Judge a Brain By It's Scan: The Importance of Actionable Information in Medical Decisions

A common and vexing problem in ICUs everywhere is posed by the patient with diffuse encephalopathy or coma - patients who are colloquially said to be "out to lunch" or "the lights are on, but nobody's home."  The underlying cause is usually a toxic, anoxic, or metabolic malady and the only available treatment is to remove the underlying insult (toxin, hypoxia, or metabolic derangement, e.g, uremia) and wait patiently to see if the neuronal injury improves or resolves.  That is perhaps the hardest part - waiting patiently, with all the attendant uncertainty and resulting anxiety, for days, or even weeks.  This, despite my knowledge that the vast majority of these patients, save for those with severe anoxic brain injury (ABI) will mostly or completely recover with supportive care and "tincture of time."  It is very difficult for me, as a physician, to watch, mostly knowing that the patient has been "out to lunch" for the past 72 or 96 hours because of drug effects, which is very common.  "Shouldn't the drugs be cleared by now?", I keep asking myself.  "Maybe I'm missing something," comes the id's reply.  This anxious uncertainty serves as an impetus for action - but what action is there to take, and is it helpful on balance?

The urge usually is to get a variety of neuroimaging tests, CT (the "donut of truth"), MRI, MRA, and probably an EEG.  But I resist this urge mightily.  These tests rarely yield actionable information - that is, data that I can act upon to change the course of care, as an alternative to waiting.  Say for example, as is often the case, the CT scan and the MRI scan are normal.  How has this helped me?  I still have a comatose patient, and I'm still stuck waiting.  (Also, without meticulous care in explaining the test's purpose and results to her family, confusion ensues.  "If the MRI is normal, why is she in a coma?" is a commonly uttered frustration.

Alternatively, the MRI can look horrible and the patient can still do very well.  I recall a case about a decade ago where we sent a patient with hepatic/toxic/metabolic/anoxic encephalopathy to "the magnet" (MRI scanner) and the neuroradiologist soon after called:  "Is this patient still alive?" he demanded.  Yes, indeed she was.  "Well she won't live long, her whole cortex is necrotic! [rotten]," he forcefully propounded.  Two days later the patient awakened.  I do not believe the radiologist's read of the MRI was in error, only that he erred in confidently inferring that function follows form.  "Don't judge a brain by it's scan" might be a useful heuristic here.  Telling this anecdote to patients' families led me to stumble upon a communication pearl:  My not getting the scan is in essence giving the patient the benefit of the doubt - because I don't want to find something that looks bad and ruins my optimism.  This is generally a very positively received explanation for families who may themselves be demanding scans, action, do something, Doc!

There are indeed cases in which radiological imaging does reveal important and undeniable information, such as stroke, hemorrhage, herniation, and swelling.  I do not impugn all scans, many times they are very useful.  I only wish to cast skeptical doubt on that large fraction of scans which are done as a pat response to non-specific encephalopathy where they are unlikely to yield actionable information.

Beyond the costs, radiation, and risks of transportation associated with the routine use of these scans, which are often not counterbalanced by the yield of actionable information, there is a psychosocial cost - in my observation, these scans increase families' anxiety.  Firstly, when you say you're going to order an MRI, false hope that we can learn what cannot yet be learned (until enough time has passed for the patient to awaken) is engendered.  The family inevitably wants to know when the MRI will be done.  The nurse says 4 PM, there are invariable delays, it gets done at 10 PM.  Anxiety pervades all of those hours.  When will it be read?  Nobody knows, but we offer "in an hour" as a guess.  More anxiety, until 1AM when the report becomes available - but it's inscrutible.  It talks of diffusion weighted this and that, and the neurologist is not available to put it into context.  Anxiety mounts.  In the morning, the neurologist attempts to explain all these little areas of this and that, or a normal scan or whatever.  But none of it tells the patient's family what they want to know, namely "Will my mom awaken?  When?"  Those questions remain unanswerable, but the family has been put on a psychic roller coaster for the past 24 hours thinking the MRI will answer them.  When it is finally done, the reason they can't divine the meaning of the scan is because there is no meaning of the scan - it is devoid of actionable information and should not have been ordered in the first place.