Sunday, December 11, 2011

Shoulder relocation - Amateur hour!

Sounds like most people have seen the website Great videos, instruction, etc. Can't recommend it enough.

But, frankly, after I've sweated and worked to reduce a shoulder using the Kocher, or Milch, or whatever procedure, and it's going nowhere, watching those videos makes me feel like a chump. Cunningham just waves his hands over the glenohumeral joint, like some sort of Australian Yoda, and Pop! Right back in.

Seriously, how can he do that?! Well, I'm working my way there, but I'm still in the realm of the Padawan, nowhere near Jedi level. So, for some ego-reinforcement, I turned to YouTube! A number of plucky DIY-ers have filmed their own approaches to shoulder reduction, and our self-esteem, if not our board-scores, stand to benefit form viewing their efforts.

In this first, it looks like the "friends" are about to apply the Spaso technique.
Ah, no.

Next, we have another example of the "maybe if we yank harder and faster" technique. The still from 0:03 tells you all you need to know about the context of the therapeutic maneuvers.
Beer? Video camera? No dislocation apparent? Go for it!

Okay, 1 last example of the "Martin Riggs" technique:
Enough negativity. You already feel that you're probably better at shoulder relocation than an inebriated crowd of adolescent males. But here are a few examples of gettin' 'er done that ought to make us feel a little humble!

This guy, likely very experienced and knowledgeable, talks hi friends through a Milch reduction:

This guy isn't quite so astute, but he gets the results he needs:

Again, the yanking. What the frak?

Lastly, this is my all-time favorite. "They just saw it on YouTube!" The reductionists start off with a brief stab at external rotation, segue into a Milch, and then, in a nod to the OG, finish off with a Hippocratic maneuver!
I like the backwards ball cap - I'm calling this the "Bro technique." Let's not try this at the "port next time you're down there!

Wednesday, December 7, 2011

Found an ECG zebra... maybe.

Quick one today.

I wasn't sure about putting the case up, partly because there isn't a tidy follow-up and definite diagnosis yet. Also because I just talked about ECGs and PE, and this is material that is done better by Stephen Smith, or at Dr. S. Venkatesan's blog. Nonetheless.

I get ECGs tossed at me all day, checking for STEMI. A number of these are on folks under he age of 40, and I admit that my guard goes down a bit when I see the age. Nothing's impossible, but... Probably not on my shift.

So the tech comes up to me, hands me the 12-lead, and says "He passed out."

Huh. This looks different.

So, when you are looking at the ECG for cardiac causes of syncope, 4 entities you cnned to consider are long-QT syndrome, WPW, Brugada, and hypertrophic cardiomyopathy. Residents are good at describing the ECG appearance of the first 3, but are a little hazy on HCM.

Well, it looks a lot like the ECG above! I'll briefly review the manifestations of HCM on the ECG, boiling down a few of the references. Speaking of which, you may do as well to stop reading this post, and just download the great article by Kelly, Mattu, and Brady. You can download it here (pdf).

A few essential facts about HCM and the ECG:

  • Most ECGs in patients with HCM will be abnormal.
  • The ECG may be abnormal even if the echocardiogram (often taken to be the diagnostic standard) is normal.
  • Signs of LVH are typical, including the high R-waves, and the concomitant ST-T wave depressions laterally.
  • Q waves are often found in the inferior and lateral leads, erroneously suggesting old MI.

These Q waves are different from infarct-related Q's, however. The are deep and narrow, and have been described as "stiletto-like." Here's an example from the Kelly paper:

Unlike ischemic Q's, the HCM variety are generally under "one small box" in width, but may be fairly deep. Deep has been defined as 1/3 or 1/4 the height of the succeeding R wave (which my guy had), or at least 3 mm in depth in at least 2 leads (ditto).

So, did he have HCM? Hard to say at this point. The patient had an echo done, and was brought in for monitoring. The echo was limited, and no "obvious" abnormalities of chamber hypertrophy or outflow obstruction were found. If I hear more about his course, I'll share it.

Friday, December 2, 2011

Not just S1-Q3-T3: Pulmonary embolism and the ECG

When it comes to pulmonary embolism, there is more to the ECG than the presence or absence of S1-Q3-T3. Hard to believe, but true! Unfortunately, none of the other signs get quite as much press.
Not helping my case.

Let me give you the conclusion of this rant up front, in case you have better things to be doing.
When you are evaluating a patient for a possible PE, there are 4 things you should be looking for on the ECG:
  1. Tachycardia
  2. Incomplete or complete RBBB
  3. T-wave inversions in V1 through V2, V3, or V4.
  4. S1-Q3-T3
 Probably there are two reasons for this relative ignorance of the utility of the ECG in this setting. The first is a sense of nihilism. For example, how often have you received a "pimping" question from an attending along the lines of "What's the most common ECG finding in PE?" The attending-dependent answer is either tachycardia, or no ECG findings. Either answer may be true, if appropriately phrased and qualified, but really, you can't win.

Reprogram the scenario?

The implicit lesson is that the ECG will not be helpful in evaluating for PE.

A second reason, at least at Yale, is that we have been so well tutored on the use of electrocardiography to assist in the diagnosis of PE that the ECG seems quaint by comparison. After all, why would you care about indirect assessments, when you can just look at the heart?

Really, which of these technologies would most appeal to the Zune generation?
The essential study to know is the Daniel paper, from Chest in 2001. You should print it up and hit a coffee shop, beacause a quick glance at the abstract is not going to do it justice, so go ahead and download it here. Now, let me set the context, because studies on PE are nuts: the evolutions in technology and prevalence are just moving along so fast, it's really hard to keep up (Like with Zunes!).

The study used ECGs that were obtained on patients who were seen in the ED, and were suspected of having a PE. In current studies, that means a d-dimer was ordered, but in this study, back in the period 1997-1999, it meant patients who had a pulmonary angiogram. The rate of positive angiograms was 43%, showing that this was a group with a fairly high pretest probability of PE.

The authors developed an ECG scoring system, based on prior literature and case series, and wanted to see how well it could predict the diagnosis of PE. The nice part is that they used EM physicians (attendings and senior residents) as the readers, not cardiologists, giving it some real-world applicability.

The first important finding is that the ECG is not likely to be the best tool for diagnosing or ruling-out PE. Tachycardia was the most significant abnormality found on everybody, PE or no. A complete S1Q3T3 was found in only 7% more people with PE than without - not real helpful.

We already knew this, but I'm just going to stop there and reemphasize this results: You can't just look at any one sign on the ECG,  S1-Q3-T3 included. It won't help you.

They ran through the results a few different ways, and it's interesting to check out all the plots and bar graphs. The money graph, however, shows how calculating the total score can be used.

Put into English:

A score of ≥10 has a specificity of over 97% for the combined presence of a pulmonary embolism with severely elevated pulmonary artery pressures. 

That's a sick, sick patient. Of course, sensitivity stinks, less than 25%, but hey.

At least one case report has highlighted this use of the ECG - when you have a high Daniel score, and for various reasons you can't get imaging, it helps justify the empiric use of anticoagulants.

Well, this study doesn't really resemble what we do today, with al these pulmonary angigrams and such, so should the results inform our current practice? Marchick decided to run all the ECGs in Kline's PERC study through the Daniel score, to see how it could help.

Remember, to get into the PERC study, a patient just had to have some test for PE ordered - CT, V/Q, US, or a d-dimer. Not surprisingly, the rate of PE found in that cohort was below 6%. This is a far cry from the Daniel study, where 43% were positive!

Using a slightly modified Daniel Score, they found that the ROC curve for the score had a area of 0.61, consistent with the original study. More importantly, they looked at the individual elements:

Both S1-Q3-T3 and T-wave inversions from V1 to V4 have an LR+ of 3.7, which makes them fairly good, but not high enough to be decisive on their own. Fortunately, per their logistic regression...

... we learn that these two elements are independently predictive, and so we can use those, plus tachycardia, to suggest a PE. (Of course, this has to be in the right context. A patient with known pulmonary hypertension from other causes will show these same signs of RV strain).

So what? you say, holding your phased array probe over the patient, blue goop running down your wrist. If you can visualize RV dilitation, paradoxical septal motion, or perhaps even tricuspid regurgitation, what use is the ECG?

Echo: Useful in the evaluation of rigor mortis.
Some folks in the ED in Florence , Italy put down their espressos long enough to investigate the incremental value of the ECG and the echo in the prognosis of PE (not diagnosis - all the patients were known to have a PE).

It gets a little complicated for my little brain, but they essentially took a group of people who had been diagnosed with PE, and looked at 3 things:
  • Which of the patients had signs of RV strain on the ECG, by Daniel criteria.
  • Which of the patients had signs of RV dysfunction on echocardiography.
  • Which of the patients had clinical deterioration or died.
So, when they boiled down the data, they found 2 important results. First, that ECG signs of RV strain are an independent predictor of clinical deterioration. It isn't a surrogate marker for echo data. Second, it appeared that signs of RV dysfunction by echo only predicts deterioration if there are already ECG signs of RV strain. 

The graph below show that echo evidence of RV dysfunction did not predict a bad prognosis unless there were coincident signs of RV strain (RBBB, T-wave inversions, etc.) on the ECG.

So, conclusion:

If you are looking at the ECG, and PE is in the differential, you need to look for all the possible indicators of right ventricular strain on the ECG. It gives you both diagnostic and prognostic information. No one will be pimping you on calculating the exact Daniel score, but you should be scanning for all the elements.

Sunday, November 13, 2011

Intraocular foreign bodies

Sometimes when I’m engaged in a “teaching moment” with a resident, a little voice will rouse itself and say “Hey! You know that last thing you said? It doesn’t sound quite right… You sure about that?” Sometimes it’s the resident saying this, of course (Looking at you, NewHavenResident!), but usually it’s my own inner voice.

I shared just such a moment with LeGrand a few days ago while we were discussing the possibility that a patient had an intraocular foreign body; the most common mechanisms, the clinical ophthalmologic exam, and the imaging test of choice. Somewhere in that conversation, I realized I was talking out of my hat. I decided a short blog post, going over some of the relevant literature, would be an appropriate penance!

First off, who gets these, and when does it happen?
Apparently, like most things in trauma, you are best off not being a young adult male. Three studies (in the UK, Egypt, and Malaysia) found that most injuries were incurred during work-related activities, and that firearms, explosions, and mowing the lawn can also play a large role.
  • Average patient is 29 – 38 y.o.
  • 92% - 100% are male.
  • In the developed world most IOFBs occur in the home (42%) rather than the workplace (33%).
  • Hammering still represents 60% to 80% of the cases.

    What kinds of things get shot into the eye? In one series of 74 IOFBs, 58 of these were metal, and 13 were glass, with only one wooden FB, and 2 “other.” A British series also found the vast majority were metal, with 9% being glass, stone, concrete, or, uh, eyelashes(?!).
    Eyelashes made of metal would explain a lot.
    The metal FBs can be drill bits, metal fillings from a lathe, as well as fragments of nails and other things you hit with a hammer. Various metals cause various problems – iron can stain the iris, copper causes a nasty inflammation, and lead can leech out sometimes.

    Other times, wood gets in the eye! Many of these FBs are from trees or branches, or are composed of some “treated” wood, which is consistent with occupational exposure. In one series, however, a third of wooden IOFBs were from pencils.
    Glass IOFBs, in one Indian series, was due to blast injury most often, as well as MVCs, and a smattering of other causes.
    Careful with your tumblers.

    What are you looking for on exam?
    So, how do you examine a patient when you have some suspicion for an IOFB? I’m not talking about the obvious cases, where you’re dialing for the on-call ophthalmologist right after you’re done with the A-B-Cs.
    "Uh, no, I haven't talked to his PMD yet..."
    Keep in mind that most IOFBs, especially glass shards, may be located in the posterior chamber, and may not be immediately obvious. A quick glance at the eyes to check off “PERRL” on the chart ain’t going to cut it – you need to bust out the ophthalmoscope, slit-lamp and fluoroscein.

    Key elements of the exam (Not exclusive).
                • Decreased visual acuity.
                • Deformation of the pupil.
                • Prolapsed iris.
                • Laceration of sclera, cornea.
                • Hyphema
                • Absence red reflex.
                • Seidel’s sign
    Click HERE to see the animation of a Seidel-positive exam. It's very cool!

    Now, if you see an FB at any point here, you’re done. Call optho, start some antibiotics, attend to the other injuries, etc. But if you haven’t found any direct evidence, you need to get some imaging. But what kind?

    Imaging for detection and characterization of an IOFB
    Plain films of the orbits are what the MRI techs ask for if there’s any history, even asymptomatic, of possible exposure to metal fragments in the past. But while they may have a place in screening low-risk patients for ferrous FBs, they don’t have much of a role in other patients.

    In one registry study, comprising both Hungary and U.S. patients, it was found that the clinical examination identified an IOFB in 46% of the patients examined, ultrasound revealed an IOFB 52% of the time it was used, and CT had 95% sensitivity when it was employed.

    A single-center study from a specialized eye & ear hospital in Ireland also looked at this question, conducting a chart review of patients with a suspicion of IOFB, who had had at least a plain film of the orbits. CT imaging of the orbits was only ordered if plain films had already been performed; only about 1 out of 10 patients went on to get a CT. Now, there was no gold standard here, and it seems like an IOFB was ruled out according to clinician judgment. Nonetheless, they found some encouraging results.
    • If there was no “clinically evident ocular penetration,” no IOFBs were found on plain film.
    • Similarly, no IOFBs were found on CT if the eye showed no clinical signs of penetration.
    • Interestingly, all patients who did have such signs either had a positive plain film or a positive CT scan.
    Given their results, they proposed a decision algorithm for imaging.

    Given the prime role that the clinical exam plays in their study results, as well as the algorithm, it is worth noting that the clinical exam these patients received went far beyond what many of us are comfortable with, including dilated fundoscopy and gonioscopy. Indeed, in the acutely injured patient, it may difficult to recognize an IOFB in the posterior chamber or elsewhere. With these factors in mind, the "EM-modified" algorithm boils down to…
    Very EM.
     Of course, in that study most of those FBs were metallic. When we look at imaging of non-metallic objects, the situation gets murkier.

    In one retrospective review of wooden IOFBs, CT was used in 22 out 23 cases. Even then, the radiologist could make a definitive call in less than 2/3 of the cases.
    "Cannot rule Ticonderoga #2. Clinical correlation suggested."
    In another study using an animal model of glass IOFBs, researchers found variable sensitivity for CT, MRI, and ultrasound in detection and identification. Interesting stuff: Detection rates were 57% for CT,  and 11% for T1-weighted MR. Ultrasound, meanwhile, found only 43% of glass fragments in the posterior chamber and 24% in the anterior chamber. On helical CT, anterior chamber glass was easiest to detect and corneal surface glass the most difficult. Sensitivity was greatest for green beer bottle glass (550 Hounsefield units!) and least for spectacle glass (around 80). So if you're going to be brawling at a saloon, take off your spectacles, and pick a beverage that comes in green glass!
    Or Heineken. Whichever.
    There are no good case series to look at the sensitivity of CT for other nonmetallic objects, but another animal model study may be helpful consider.  Researchers from Palermo used a pig model of the eye embedded with various materials, as well as injected air bubbles. The Italians found that the plain films were variable for detecting IOFBs, usually missing plastic or wooden objects. MRI was disappointing, showing significant artifact when examining objects made of  graphite, glass, and especially iron. The CT, however, was always able to “detect and differentiate” IOFBs.
    • Row A - Plain film
    • Row B - CT
    • Row C - MR-T1
    • Row D - MR-T2
    • Arrow = FB or air; arrowheads = lens; double arrows = optic nerve.

    But what about ultrasound?
    Ultrasound has some strong potential attributes. No radiation, no worries about jostling ferrous FBs around the head, and the patient isn't out of the department.

    And there are some encouraging studies to point to. One porcine model study found the technique to quite accurate, and found sensitivity to be 87%, and specificity 96%. However, the metallic fragments were introduced into the vitreous of the pig eye, whereas IOFBs "in real life" may not be as evident.

    This may be especially true with non-metallic objects. In the Indian study that surveyed their experience with glass IOFBs, the researchers noted that ultrasound could not detect the glass fragment in about 25% of patient. Typically the shards were located in either the anterior vitreous or ciliary body area. Artifacts from vitreous hemorrhage, lens opacities, or choroidal detachment also made for challenging ultrasound exams.

    A frequent concern about employing ultrasound, for whatever goal, is that it requires skill, and is (gasp!) operator-dependent. It was heartening to read one paper, then, that took on the issue of skill acquisition head-on. The authors of "Ultrasound detection of simulated intra-ocular foreign bodies by minimally trained personnel" wanted to see if they could teach 4 NASA astronauts to perform ocular ultrasound to a level comparable with a group of expert sonographers. They used a gelatinous ocular model embedded with various size pieces of metal, plastic, and glass.

    They are to be commended for taking the study to the obvious next level, and enrolled 10 high-school students in the study. I think you can guess where this is headed; the astronauts and high-school kids both got pretty good at picking out FBs, both groups demonstrating equal sensitivity and specificity, and not to far behind the experts!
    To be fair to John Glenn, they were from an AP biology class.
    Nonetheless, real-world use of ultrasound shows lower effectiveness. It's important to emphasize here that you should not be ultrasounding any eye that shows signs of a globe perforation, as the pressure of the probe could extrude contents. Furthermore, recall that a registry study mentioned earlier only found ultrasound to be 52% sensitive, far lower than CT. Now, ultrasound was only conducted when posterior chamber FBs or pathology was suspected, and likely was only employed if the object was not visualized on exam. Thus, the patients in whom ultrasound was the most appropriate were also patients in whom the exam would be more difficult!

    Take away message
    It may be surprising, after all that, to come to the nuanced conclusion:

    Just scan 'em.

    Thursday, November 3, 2011

    Benign early repolarization

    A few days ago I was just about to walk out of the pediatric ED, when the tech handed me an ECG: "I need you to look at this right now."

    All caps = important.
    All caps + asterisks = very important.

    Ah. I see. 
    The patient turned out to be a very healthy looking, comfortable, 28 y.o. African-American male, and he happened to have an odd chest discomfort, "like needles." He actually wasn't having the pain at the time the ECG was taken.

    Despite the dire diagnosis on the EKG (Thanks Marquette!), he walked out of the ED a few hours later, after multiple negative cardiac enzymes, sequential ECGs, a bedside echo, as well as a turkey sandwich. However, his favorable course could have been predicted from the classic findings on the ECG, diagnostic for benign early repolarization (BER).
    First off, before we review the criteria for BER, note that there are no reciprocal changes in the ECG, which would be extremely unlikely in a massive ***ACUTE MI***. Right off the bat, you know this is far more likely to represent a mimic of some ilk. 

    So, widespread ST elevations without reciprocal depression, there are 2 possibilities in the differential. Pericarditis is one, but a few things mitigate against it. There doesn't appear to any PR depression (or any PR elevation in aVR), and the T waves are all upright. So, possible, but not not clear.

    Now let's take a look at the criteria for BER.
    This table comes out of the excellent review article by Brady and Chan (1999) (Download pdf). Looking at the ECG, we see ST elevation in leads I, II, aVL, and V2-V5 - certainly very widespread, with elevations in the precordial leads looking more prominent than the limb leads. 

    Next, we note that in leads II and V5, where the ST elevation isn't that pronounced, there is nonetheless a notable elevation of the J-point, that place where the QRS "meets" the ST segment. 
    Lead II, showing J-point elevation over 0.1 mV
    Also note that none of the complexes with ST segment elevation show convex-upward segments, but instead concave-upwards morphology.

    Note also that the J-point in the ECG doesn't show a clean transition from the R wave to the ST segment. Rather, there seems to be a messy transition, either a "slurring" or a notched junction. You can see the slurred J-point in the blow-up from lead II above, or take a look at lead V4:
    Notched J-point
    As noted before, the T-waves are all appropriately upright and quite prominent. As for the other criteria, they're difficult to judge on a single ECG!

    Who has BER? Well, this patient was classic for the epidemiology of BER, being young, fit, male, and African-American.The pattern is found very often in male athletes, and appears to have no connection to HCM, or any other causes of sudden cardiac arrest.

    My philosophy is that the emergency physician needs to be competent in many spheres, and across many disciplines. However, in a few areas we need to be the experts in the hospital, and reading ECGs for signs of acute ischemia, or its mimics, is such a skill. In training we study more ECGS than anybody in any other field. And when you're an attneding in the ED, it's just one after another... All that training and repition pays off - In one study, Turnipseed et al. showed that EPs could read BER versus AMI on the ECG just as well as cardiologists, if they corrected for years of experience. (download pdf)

    See you in room 4!

    Tuesday, October 25, 2011

    Idiopathic Intercranial Hypertension; neither pseudo nor benign...

    Doug, sorry I had so few answers for you in the ED. Had to go hit the books after we had that patient!

    This isn't a comprehensive article on IIH, nor is it an efficient outline of the critical information for the boards, life, or pimping. It's just a list of 5 things that took me somewhat by surprise, that I had never learned, or that I swear I had learned as the opposite.

    1. "Transient visual obscurations" - The predominant visual disturbance isn't a nice, clean visual field cut. Instead, over 70% of patients have really brief episodes (< 1 minute) of loss of acuity, provoked by standing, sitting, light, Valsalva, or extra-ocular movements. Yeah, you'll get field loss on perimetry, but the TVOs are what patients will actually complain of.

    2. Sparkles - They can also get flashes, or photopsias, as well as the TVOs.They are described as "white or less commonly coloured small flashes, flickering lights, stars twinkling, or flashes in the periphery of the visual field
    Simulation available

    3. Patients with IIH also report an odd kind of noise inside their heads. It's termed "pulsatile tinnitus," but it only infrequently seems to be a high-pitched tone. More often, it's described as '"a rushing river', a waterfall or a buzzing, whistling or blowing sound."

    4. You get imaging to r/o something else, like a not-so-pseudo tumor or a sinus venous thrombosis. It's not used to diagnose IIH. However, one finding that would be consistent with IIH would be small ventricles or an empty sella,  according to some.
    Flattened ventricles.

    5. Perhaps the imaging study that we should be using more often is our ultrasound. Up until this month, the world's literature for using ultrasound to detect papilledema was limited to this study by Michael Stone (Download). While the case provided an example of using an optic nerve sheath diameter of >5 mm  to make a diagnosis of increased ICP, it also demonstrated sonographic papilledema.
    3mm posterior to the retina, check for OSD  > 5 mm.
    Also note optic disc elevation.

    But now there are 2 new publications that provide more evidence that we should be dropping our old clinical skills (polished as they may be...) in favor of using newer technology!
    1880 Loring opthalmoscope. Not new.
    The first article is an abstract that was just published in the October issue of Annals of Emergency Medicine, the ACEP Research Forum 2011 supplement, and is entitled "Point-of-Care Ocular Sonography to Detect Optic Disc Swelling." (Download pdf)

    The authors compared EP-performed ultrasound exams of the optic disc with those of an neuro-ophthalmologist, as well as optical coherence tomography.
    Optic disc swelling as seen on OCT
    For the study,  2 EPs hung out in a neuro-optho clinic, and did ocular US on a number of patients. They later compared their results with the specialist, who also had access to the OCT images and results. After 20 patients, they found they had "excellent correlation" between the OCT and height of the disc seen on ultrasound.
    Another example of an elevated optic disc (small arrow)
    Another article, still in-press at the American Journal of Emergency Medicine (by Daulaire et al.) (Download pdf), reviews a series of 3 headache patients who had apparent optic disc elevation on bedside US. The US results were considered confirmed, in each respective case, through a finding of elevated CSF pressure, an exam of the fundus by the ophthalmology service, and an MRI. There's a review of the technique, as well as of the scant literature.

    So, the next time you have that odd headache patient, ask them about TVOs and photopsias, and put a probe on their eyes!

    Saturday, October 22, 2011

    Cervicitis and PID

    It has come to my attention that the tenuous grasp I thought that I had possessed about cervicitis and PID became archaic at some point. My beloved, and much highlighted, text that was new when I started med school is now behind the times.
    It is so 2004...
    To be fair, the 2000's have been active in this area, and I think that you should hear a little bit about what's been goin' on. 

    First up: What are cervicitis and PID, i.e. what are the diagnostic criteria? This is important, because it turns out that in the ED we aren't so hot with the diagnosis of such things. Two studies point this out.
    That's pus.
    This study done in the Yale ED was written by your current boss (and with a future boss?), so you should probably know this! 
    The paper, "Compliance with the CDC Recommendations for the Diagnosis and Treatment of Sexually Transmitted Diseases" (Download here), published in 2004, documented how essential elements in the history and physical exam where missing from the charts of patients who had been diagnosed with cervicitis or PID. Furthermore, incomplete or erroneous treatment was often provided. All in an ED we all know and love...
    More pus in dere (PID).
    Another study, hot off the presses, make same case. (For download: Cervicitis in Adolescents: Do Clinicians Understand Diagnosis and Treatment?) Folks from the urology department at the U of Arkansas reviewed charts from both a primary care office and from a children's ED. All the records of adolescents who had received a diagnosis of cervicitis were analyzed for elements of the history, physical exam, and treatment. 

    First off, about 25% of the patients diagnosed with cervicitis did not have documented physical findings that supported the diagnosis; i.e. they had neither a mucopurulent cervical discharge, nor a friable, easily bleeding cervix. Despite this over-diagnosis, they also found that 40% of the women who had been diagnosed with cervicitis actually had sufficient exam finding to meet PID criteria. So, they were also under-treating! Urgh. 

    Even better, they break the results down according to the site of treatment: the adolescent clinic or the children's ED, and no one comes off looking good. The ED misdiagnosed about half the time, and the clinic about a third.

    So, let's get the definitions laid out, so there is no confusion. This all comes from the current CDC guide for STDs, which you can access online, or you can download the pdf.

    "Two major diagnostic signs characterize cervicitis: 1) a purulent or mucopurulent endocervical exudate visible in the endocervical canal or on an endocervical swab specimen (commonly referred to as mucopurulent cervicitis or cervicitis) and 2) sustained endocervical bleeding easily induced by gentle passage of a cotton swab through the cervical os." 

    "Empiric treatment for PID should be initiated in sexually active young women and other women at risk for STDs if they are experiencing pelvic or lower abdominal pain, if no cause for the illness other than PID can be identified, and if one or more of the following minimum criteria are present on pelvic examination:
    • cervical motion tenderness
    • uterine tenderness
    • adnexal tenderness."
    They note that in cases where a diagnosis based on these minimal criteria "might cause unnecessary morbidity," that a few other elements may be used to boost the specificity, namely a mucopurulent discharge or a fever.
    Telling this guy that his 14 y.o. daughter has PID = morbidity?
    By contrast, the 1998 CDC guidelines required that all 3 of the minimal criteria (CMT, uterine, and adnexal tenderness) be found in order to make a diagnosis. Why did this change? After all, it's not so often that we change a diagnosis. Femur fractures, for example, have never had a revision of the diagnostic criteria!

    Well, the PEACH trial happened. (Download here
    This was a major randomized trial, and I simply will not do justice summarizing it here. Instead of reading any more mind-numbing studies about subarachnoids or PEs, read this. 

    The trail was designed to examine the effectiveness of IV versus outpatient treatment of PID, but since they were collecting all this data on women with suspected PID, and then getting all these confirmatory tests, they wanted to see how sensitive and specific the elements of the CDC diagnostic criteria were. It was a multicenter trial, in both clinics and EDs throughout the US. Diagnostic techniques were comprehensive: PID was diagnosed histologically, from samples obtained from transcervical aspiration of endometrial tissue. In the end, they had complete information on 651 women, and the results were...
    They found that the minimal CDC criteria (all 3 of CMT, adnexal, and uterine tenderness) was only 83% sensitive, with a specificity that wasn't exactly a selling point. Furthermore, if you were hoping that supporting elements, such as a fever (or it's absence) might help diagnosis, there were disappointing results.
    For my part, the negative likelihood ratios for fever and purulent discharge grab my attention. The absence of the elements does not meaningfully help the diagnosis, since the negative LR is close to 1. Heck, even a negative NAAT test only cuts the probability in half!

    In the discussion section, the authors offered their suggestion that "clinicians should consider empiric treatment of pelvic inflammatory disease in at-risk women with adnexal tenderness at presentation and no other obvious diagnosis," which is close to the current guidelines. And even with this incredibly liberal definition of PID, we are still going to miss about 5%!

    So that's it for diagnosis. As for treatment, like all of ID, things change every year - look up the current reccs in the CDC guide I linked above. Some things are suprising (no more 125 of Rocephin!), and others stay the same (7 days of doxy for cervicitis, 14 for PID).This post is long enough, so I'll leave you with just one more cervix:

    Thursday, October 6, 2011

    2 important points about treating ACS

    I wanted to quickly review 2 issues that come up with regularity when a resident & I have a patient with ACS, either a STEMI or NSTEMI. Let me start with the conclusion first, and go from there.

    1. Tachycardia is a reason not to give IV beta-blockers in the ED for NSTEMI or STEMI.
    2. Heparin hasn't actually been shown to have much effect in NSTEMI.

    Okay, first about the beta-blockers. There used to be a lot more enthusiasm for using IV metoprolol in the ED with a STEMI, and many clinicians still feel that they are obligated to give them. But a lot of that changed, first when the COMMIT trial came out, and then when the AHA modified their guidelines to reflect the new evidence. In that big trial, patients with a STEMI were given the IV metoprolol load in the ED, followed by PO. The kicker is that there was overall no difference in 28 day mortality, since for every person who apparently didn't have a reinfarct or fatal arrhythmia. there was an extra person who died of HF!

    Make special note of the risk factors listed after the asterix, in small print, at the bottom: sinus tachycardia exceeding 110 bpm.

    These considerations were extended to the NSTEMI guidelines as well, although the evidence base is not as direct or contemporary as it is for STEMI. The 2007 AHA UA/NSTEMI guidelines basically mirror those for STEMI with regard to PO beta-blockers (Class 1 in the first 24 hours) and IV beta-blockers (class 2a, with same contraindications as above).

    As for heparin for NSTEMI, it is sort of absurd looking at the recommendations and the supporting evidence. The 2007 AHA UA/NSTEMI guidelines cite 2 studies in support of the use of UFH. The more recent, and larger, was  this paper , a meta-analysis of 6 studies that looked at the benefit of adding heparin to aspirin in UA/NSTEMI.
     Ok, look at the title. Seems like a pretty clear title - you know just what they found in their study, and you should expect to find at least statistical significance in the results, right?
    Not really
    Right there, first page - the RR for MI or death was not significantly reduced when heparin was added to aspirin. They include this helpful graph, which shows the results of 6 trials, and the summary estimate that they calculate.
    In the last few sentences, the authors, note that "this meta-analysis of 6 randomized controlled trials demonstrated a strong trend toward reduction in risk of MI or death during randomized therapy in patients with unstable angina treated with aspirin plus heparin compared with those treated with aspirin alone." The phrase "strong trend" is not found in the conclusion of the abstract, but instead they highlight the "33% reduction" in outcomes. 

     Heparin probably has utility in the sicker subset of NSTEMI, the patients with positive enzymes, dynamic ECG changes, ongoing pain. But those are the kind of patients you're talking about with the cardiologist, calling CCU, and perhaps arranging same-day cath lab evaluation. But for the run o' the mill ACS patient, check out the evidence first.