"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.