If there’s one thing that all Sci Fi nerds should know, it’s the catchy catchphrase of the cybernetic hive mind of The Borg – “Resistance is Futile”. True aficionados will recall the battle for Earth after the defeat at Wolf 359, where Captain Picard, captured and now “Locutus of Borg” was used by the Federation to destroy the Borg cube and save the Earth, proving that resistance, after all, was not futile.
In the same vein, many people view treating bacteria resistant to antibiotics as a futile endeavor. But it’s not as simple as all that. In order to understand why, we have to break down what it really means when we label a bacterial isolate as “Sensitive”, “Resistant” or “Intermediate”.
The core principle of bacterial resistance is the MIC, or minimum inhibitory concentration. The MIC is the concentration of a drug that will inhibit growth of that bacteria in the lab, in the old days tested using doubling-dilutions of drug and seeing which test tube the bacteria first grew in. The MIC was the dilution above that level (so if bacteria grew at a dilution of 1:32 but not in 1:16, the MIC would be 1:16). You can then give that value in terms of milligrams of drug.
Now, here is the key point. When we state that a particular MIC corresponds to being “sensitive” we mean that for THAT BUG and THAT DRUG it will kill the organism in the BLOOD, assuming normal dosing.
MICs cannot be compared between bugs. And more importantly they can’t be compared between drugs! You should NOT pick your drug based purely on the MIC that the lab reports out. In fact, a good lab will not report out the MICs, but will instead simply interpret them for you to say sensitive, resistant or intermediate (a weird concept, where the MIC is neither high enough to be considered truly resistant, but not low enough to be truly sensitive either – a clue that it isn’t a black and white interpretation). Unless you’re an ID doc or a pharmacist and you know what you’re doing, you have no need to know the MIC at all. The choice of drug should be based usually on the class of drug, and the location and type of infection you’re dealing with. I’d rather use oxacillin to treat staph with an MIC of 2 than vancomycin for the same infection with an MIC of 1, and I’d certainly never use rifampin by itself despite a potential MIC of 0.03.
If the infection is in a different body location, especially somewhere like the spinal fluid or brain where the blood-brain barrier can prevent drugs from getting in, then the MIC doesn’t apply. If only 20% of your blood level of drug gets into the spinal fluid, knowing that your bacteria is “sensitive” to blood levels isn’t entirely reassuring. In fact, for some bacteria the lab will report out separate “meningitis” MIC levels to take this into account, and many drugs have “meningitic dosing” which is much higher that normal dosing (remember, sensitivity MIC refers to that bug, that drug, in the blood, using normal dosing). Some drugs don’t even get into the spinal fluid at all – you’d never use cefazolin to treat staph meningitis for example, although for almost every other type of infection it’s one of the best anti-staph drugs out there.
The opposite may be true for urinary infections, as many drugs are concentrated in the urine, so urine levels may be 10-100 times the blood level, and even “Resistant” organisms will be killed.
But when you’re faced with a nasty bloodstream infection, or a pneumonia, or cellulitis where the MIC is probably helpful enough, and it’s resistant, what can you do?
It can depend on the resistance mechanism. Streptococcus pneumoniae has an altered binding protein, so simply swamping the bug with excessive penicillins might be enough to work. Staphylococcus aureus has a beta-lactamase that will destroy basic penicillins, and adding a beta-lactamase inhibitor will defeat that mechanism, or moving to a higher class of drug like a cephalosporin (first generation, of course).
But what about tougher bugs with weird mutations, pumps that remove antibiotics from the bacteria or porin mutations that prevent the antibiotic from getting into the bug in the first place? Sometimes a higher dose by itself isn’t enough. With some of the beta-lactam drugs the important concept is “time above the MIC” rather than sheer dose of drug. If the MIC is 32 but you can get blood levels of 33 for 24 hours a day using a continuous infusion, that will be enough to kill the infection, even though using traditional dosing that would be considered resistant. Prolonged infusion is a halfway house to try to achieve the same end, and can also be used to extend the total exposure of the organism to the drug “area under the curve” of a graph of drug concentration over time. And you can also simply use higher doses, assuming the drug isn’t toxic enough to limit that approach.
Incidentally this is why vancomycin is a crappy drug – sure, it kills MRSA, but the limits between effective and toxic are quite narrow, and you can’t increase the dose much at all without dinging the kidneys.
Another approach is the use of multiple drugs at once, targeting different bacterial biologic mechanisms. Intuitively it makes sense – attack the cell wall AND protein synthesis, or DNA replication, and you ought to kill it off faster. Often this approach is not simply additive – there is synergy between the two drugs such that 1+1=4 when it comes to killing ability. Relatively inactive drugs like the aminoglycosides (gentamicin, tobramycin) or rifampin, can be very effective when paired with a beta-lactam or other cell-wall agent. I call them the SALT drugs. Synergistic Although Lousy Therapeutically. And you’d never eat salt by itself, always with something else….unless you’re a goat.
One very interesting report of lab work with an old drug called colistin and vancomycin showed that if you put the two together, vancomycin could be effective against bacteria that it would normally have no activity at all against. The colistin punched holes in the bacterial membrane that allowed the vancomycin in to act on the inner cell wall. (WARNING – lab report only, do not try with real patients….yet…).
So when we are faced with resistant organisms, it’s never truly a totally lost cause. There are always ways to try to optimize either the dose or the timing of doses to keep drug levels up, or combinations to try, or novel ideas. But there’s no guarantee of success, in the same way that even with sensitive bacteria there are still going to be treatment failures.
Ultimately we need new drugs, and new drug classes. If we have to go up the development chain to counter old resistance mechanisms, all we’re going to go is promote the evolution of new resistance mechanisms. Even the newest anti-MRSA 5th generation cephalosporins are modifications of penicillin, when all is said and done. We really haven’t come very far at all.
I joke that, as a Peds ID doc, it is my duty to say this at least once a day…
Ok, I may not literally be slapping people upside the head, but there are certainly times when I’m doing it in my mind. The situation is common enough – a patient, parent or doctor, faced with symptoms consistent with an infectious disease, considers using antibiotics to treat bacteria. After all, we know that bacteria kill people, right? But in many of these situations the patient really has a viral infection – and viruses aren’t affected by antibiotics. So at the very least we’re wasting money and drugs. Worst case scenario? We’re promoting drug-resistant bacteria, antibiotic allergies and side effects – that in some cases can be life-threatening.
But aren’t there clues to help us make the distinction? Real clinical signs and symptoms? Well, lets review a few.
White pus on the tonsils
Everyone is familiar with the feeling of an awful sore throat, and having a doctor peer down and having you say “Ahhhh…” What are they looking for. Probably something like this:
This is a classic appearance of “Strep Throat” – a bacterial infection that aside from being painful in its own right can go on to lead to serious complications, such as rheumatic heart disease, kidney disease, a form of arthritis and a weird neurologic disorder called “Sydenham’s Chorea”. Fortunately it has no drug resistance so simple penicillin/amoxicillin will kill it (so if your doc tries to give you “stronger” antibiotics please feel free to slap them).
The trouble is, this isn’t a picture of strep throat. I grabbed this from an article on “Mono”. Infectious Mononucleosis can be indistinguishable from strep throat, but antibiotics do nothing for it. The “pus” you see isn’t really pus, it’s just a nasty-looking white gunk your tonsils make. A bad sore throat can be caused by influenza, adenovirus, RSV, metapneumovirus, rhinovirus….you get the idea. It can be hard to tell strep throat from any of the other many possibilities, but in general if you DON’T have a runny nose or a cough, and the lymph nodes in your neck hurt then it’s PROBABLY strep. But it could be a virus. Strep tests and cultures help – and holding off on treatment until the test comes back is a sensible plan.
What about ear infections? Another common bane of pediatrics (almost every young child I see with a prolonged illness has at some point been diagnosed with an “ear infection” before arriving at the correct diagnosis – I once saw a kid with a brain tumor get that diagnosis…). The symptoms are notoriously non-specific (ear pulling, fussiness, fever) and a good ear exam in a small, squirming child can be difficult! A crying baby can turn their ear drums pink…and voila! An ear infection! But even assuming your exam is good and the ear drum really does look nasty, how do we know its a bacterial infection? Despite the appearance of a rip-roaring otitis media (bright red, bulging ear drum, fluid behind it) it can be a viral infection too. Most of what you see is the BODY’S response to the infection remember. Clinical trials of antibiotic use have shown with without antibiotics, ear infections tend to get better just as quickly as with them. Complications from untreated bacterial infections do exist, and can be quite serious, but are rare. It is prudent to consider a “wait and see” approach to ear infections to see if it gets better by itself. I don’t want your kid to get mastoiditis any more than you do, but if it does happen I want it to be treatable with the best antibiotics!
Most of the time when we’re treating ear infections we’re not even treating the child…we’re allowing the adults in the house to get a good nights sleep…;-)
Cough, fever, patches on chest x-ray
Pneumonia? Guess what. Usually a virus, at least in kids, before they become immune to everything. Without proper testing though this can be harder to tell apart, and we’re getting into the realm of “sick kid” here. Almost every doc will feel a little weird ignoring a possible bacterial pneumonia, even if they really do think its viral. But the high rate of viral infections, along with the risk of increasing drug resistance, is why the current recommendations for antibiotic treatment of pneumonia in children start with plain old amoxicillin. RSV, metapneumovirus, influenza, adenovirus – they can all cause pneumonia. In the Bad Old Days viruses like measles and varicella could also do it, and they were quite nasty! With symptoms like a runny nose, rash, lots of sick contacts, the chances of it being a viral infection are quite high. Sitting it out for a few days is again a reasonable option – because you know if you see a doc and get a chest x ray they’ll start you on antibiotics, and we don’t want that, right?
Very high fevers, difficulty breathing, chest pain with pneumonia, coughing up junk – always worth getting checked out.
All of us have at some point experienced symptoms of a sinus infection. Fever, pressure, tons of snot, headache. They are truly miserable things. I hear all the time how “we knew it was bacterial because he had green snot”. Sorry, but that’s not all that helpful. The greenness of snot comes from the cells your body is sending in to kill the infection, which will tend to be neutrophils whether it’s a virus or bacteria. (Neutrophils don’t really kill viruses, but they’re just reacting to the inflammation there). Neutrophils have the awesome ability to create highly-reactive chemicals, one of which is called “superoxide” which gets converted to hydrogen peroxide which then reacts with chloride ions in salt to produce….bleach. The green color you see is actually the neutrophils and the enzyme they are using to create the bleach (myeloperoxidase), not the infection itself. You’ll get green snot regardless of what’s causing the infection, and it’s a good sign – a sign that your immune system is in full swing.
Severe sinusitis will produce lots of snot, for sure, but lots of snot doesn’t necessarily mean its a severe sinusitis, and certainly doesn’t prove it’s bacterial. If symptoms have lasted for a couple of weeks with no improvement, that’s a red flag for something non-viral.
Fever is a normal immune response which effectively suppresses bacterial and viral infections. It hurts them far more than it hurts the patient. A fever by itself won’t necessarily cause any harm at all – and high fever may or may not indicate bacterial infection. A fever is just a clue – a reason to look and figure out what’s going on. One you’ve figure out it’s a virus based on symptoms (runny nose, viral rash etc) then you’re good. And don’t worry if fever keeps coming back, it will do that until the infection is gone, which may take a week or more.
The height of the fever is only slightly predictive of the risk of bacterial infection – but influenza, adenovirus, EBV can all cause pretty good-going fevers of 102F and up. I’m far more interested in what ELSE is going on in addition to the fever.
Febrile seizures, convulsions caused by fevers in young children, are more closely associated with a rapidly rising fever than a high fever itself. If your child has a fever of 104.5F and has sat there for an hour, chances are good they’re not going to seize from that.
Addendum – Mark Crislip recently posted on fevers over at Science Based Medicine!
So that’s a rough overview of the various common viral infections. It really is surprising how often we do get sick from something that will simply run its course. Our immune system is pretty robust. That’s not to say that in exceptional circumstances viruses can’t or shouldn’t be treated (herpes, influenza, chickenpox, measles, adenovirus, CMV and EBV all have some form of treatment to try even if the therapies are nowhere near as effective as antibiotics are on bacteria) but for respiratory infections in particular we would be far better served by reassurance that our symptoms are more consistent with a virus than a bacteria, and that most of the time it will sort itself out. A large chunk of the inappropriate usage of antibiotics stems from over-treatment of viral respiratory infections – so next time you see your doctor for something like this consider asking about tips for symptomatic relief rather than an antibiotic prescription.
A few other studies: prescribing antibiotics doesn’t necessarily save time.
Antibiotic overuse, even based on physician diagnosis, worse with criteria-based diagnosis.
Understanding why physicians overprescribe – many different reasons.
Good advice can be found on the CDC website.
I have been told that I must credit my wife for originally coming up with the idea for the “IT’S A VIRUS” slapping Batman meme, and Quickmeme helped me create it.
Ermahgerd! It’s MIRZAH!
MRSA, affectionately pronounced “mur-sah”, and the abbreviation for “methicillin resistant staphylococcus aureus”, has become the epidemic of our time.
Everyone thinks they know what it is. Few actually have a good handle on what it really means, especially with kids.
MRSA was first described back in good old Blighty in the 1960′s, not long after the drug methicillin was released in an attempt to combat the rise in penicillin-resistant staphylococcus aureus. In the modern era methicillin is no longer available, due to kidney toxicities that are much less in the current selection of anti-staph penicillins (nafcillin and oxacillin), but the MRSA tag remains in use.
In practical, and literal terms, it simply means that the organism in question is resistant to that particular antibiotic. Well, whoopdedoo. Lets just pick another. Except you can’t. The way in which staph becomes resistant to methicillin is through the production of an altered protein that renders the bug resistant to EVERY antibiotic in that entire FAMILY of antibiotics. Penicillin? Gone. Cephalosporins? Gone. Beta-lactamase inhibitors? Useless. Carbapenems? Fat chance.
So you go to another class – quinolones, aminoglycosides, tetracyclines, sulfonamides – but none of them are especially active against staph and…wait for it….MRSA is often resistant to these drugs too.
The first place in which MRSA was discovered was in healthcare settings – long-term care facilities and hospitals. The overuse and abuse of antibiotics selected for strains of bacteria that had acquired all sorts of resistance genes. In fact, the gene for hospital-acquired MRSA is a multi-segment behemoth that carries with it all sorts of additional genes, so the whole lot are inherited together. MRSA infections were associated with severe, invasive disease and death, usually in adults already weakened by other diseases. Due to delays in starting the right treatment, and being forced to use second-line, less effective drugs like vancomycin, MRSA infections add to hospital stays and healthcare costs. Like to the tune of $60,000 apiece.
Just as the world was getting used to dealing with MRSA in hospitals, we started hearing about it in the community. People were showing up with skin abscesses, boils and other infections that were, in about half of cases, growing out MRSA. Worse, they didn’t seem to have any link to the typical risk factors of diabetes, renal failure, cancer, prolonged hospital stay etc. And even more scarily, this was being seen in kids.
But they’re different from the old hospital-acquired MRSA cases. The community MRSA gene cassette is far smaller, lacking the resistance genes of the hospital MRSA. We have a small, but reliable list of antibiotics to use to treat it. Invasive disease is unusual, skin infections are the norm. I have not, yet, seen a real hospital-acquired strain of MRSA in a child. I have seen a few kids pick up MRSA while in the hospital, but it’s always been the “community” strain brought in by visitors, family or other patients.
Diagram of MRSA gene cassettes – hospital (top, types I thru III) versus community (bottom, types IV thru VI)
Right now, I see a steady stream of kids with MRSA in my clinic and in the hospital. By far the vast majority are recurrent skin infections, often bouncing around various family members. Parents, reading up on MRSA online are understandably freaked out. Friends and relatives shun their kids, for fear of picking it up. Furnishings and furniture are steam-cleaned and thrown out, course after course of an antibiotic is given to treat each infection, but they never seem to go away. Even pets end up getting “swabbed” and tested in the lab, and yes, some are sent on their way as the presumed culprit.
None of this matters.
The truth of the matter is, while MRSA does indeed cause a good chunk of these kind of infections, it’s not got the hold on it. Just as many regular, sensitive staph (MSSA) cause these things. Fully one third of the population carries staph aureus on them – and clearly one third of the population is not suffering from recurrent skin infections. Carrying staph doesn’t mean you’ll get infections. And, annoyingly, you can test negative for staph from a swab (typically done from the nose) and still have infections elsewhere, such as the armpit, legs, or buttocks. We’re exposed to staph everywhere, all the time – and we mostly don’t even know it. That’s if we don’t have it already.
The reason why the skin infections keep happening is due to an entirely separate set of genes, related to immune evasion and skin invasion, which although more common in MRSA are also in some MSSA. (They are, interestingly, mostly absent in the hospital MRSA strains.) The way to get rid of it, if the levels are high enough for these infections to keep happening, is simply to decolonize the skin. That can be done with chlorhexidine washes and bactroban nasal ointment (a two week protocol), but you also have to prevent re-colonization, a more difficult proposition. Bathroom surfaces need to be bleached, towels washed daily (paper towels for hand washing) and EVERYONE in the household needs to have this done. There’s no point focusing on little Johnny with his butt abscesses if mommy and daddy, who are carriers, give him a hug and spread it back.
I never promise that with this approach staph will go away entirely. What we do know is that, if everything is done at once, you CAN eradicate staph at least temporarily from the skin. What we also know is that a third of the population carries staph….so wait long enough and you’ll get it again. I hope to merely reduce the frequency of outbreaks.
In my experience…this seems to work. Except in situations where kids have severe eczema or other skin issues, or where they’re not following EVERY step of the plan, I generally don’t see these kids back again.
So that’s prevention – what about cure? How should we treat these kinds of infections when they do show up? One drug that has seen a resurgence of late is bactrim – trimethoprim-sulfamethoxazole. A combination drug that is designed to inhibit the bacteria’s use of a chemical called folate which is a key component of DNA creation. It sounds good on paper, stop the bacteria from growing and it’ll die. In the lab, staph is often 99% sensitive or more (good odds when your risk of resistance to other staph drugs is around 50%!). The trouble is, in an abscess there is pus. And pus is basically dead and dying cells and bacteria. That’s a lot of DNA hanging around. Using bactrim in that setting is a lot like telling a farmer he can’t grow any more food, but putting him in a grocery store. He ain’t gonna starve any time soon. Bactrim also ignores the risk of strep, which are the other cause of skin infections and which are inherently resistant to bactrim. As such, deliberately targeting MRSA with this kind of approach actually results in MORE treatment failures than using a simple staph drug like cephalexin, even though that shouldn’t work with MRSA! You WILL get treatment failures with cephalexin too of course, and some with the other drugs like clindamycin, doxycycline etc. But it’s as if one should ignore the MRSA when planning your treatment. Drain abscesses (you usually don’t even need antibiotics if you do that) and then use a regular “skin infection” drug to minimize side effects and maximize your chances of success. These days we have NO ideal drug for empiric therapy of skin infections – but we certainly do worse if we panic about MRSA and try to tackle that first. Weird.
Of course sick patients are a different matter – even though the risk of severe invasive disease is low, the consequences are dire. You should ALWAYS cover a very sick patient with vancomycin or other MRSA drug until you know what you’re dealing with.
So I don’t panic about MRSA. I see it all the time. It’s annoying. It’s rarely dangerous. I know that if you focus on it to the detriment of the regular staph and strep you do worse. If someone is a carrier or has an active infection, good hand washing and covering any draining sites is enough to keep it at bay. No need to decontaminate entire schools just because a kid has been found to have MRSA. No need to put everyone on vancomycin if they’re not sick. And if they ARE sick, please don’t use vancomycin by itself, cos its a crappy drug and we only use it because we have to. Don’t bother swabbing just to check for carriage – positive results aren’t worth acting on unless the patient is sick (or, perhaps, due for surgery soon…that’s a whole other issue), and negative results are useless if the patient is actively infected. Deal with the infections, attempt decolonization, move on. Repeat if necessary.
MRSA – it’s a pain in the butt. And not just for the patients.
Today I had the privilege of being the very first doctor at my hospital to see a patient, document the visit (including a history and exam), write a note to the referring doctor, and complete my billing, using our new electronic medical record.
The build up to our new system has been over many months. Behind the scenes our IT dept has done its leg work, negotiations, analyses, and picked out what it hopes will be the best solution for us moving forward.
To be fair, we’ve had a semi-EMR already – a hodge-podge of software systems that barely talk to each other and seemed to have near-daily issues or crashes. My dictated visit notes were in one system, labs were in another, x rays in yet a third – and paper charts to top it off.
Not any more.
The new system will, eventually, replace all of this – and more. Our scheduling software is integrated, billing is integrated, all results are there alongside (indeed linked to) the visit they were ordered at, and every subspecialty will see what every other speciality does, including inpatient wards and the ER. Prescriptions will be faxed to pharmacies. Patients will be able to access their records online. It will be awesome.
There is, however, a learning curve. It’s not only a new software package after all, in many respects it’s an entirely new way of thinking and operating. For some Docs their work flow will be significantly altered, but it’s a fairly flexible system. It can handle point-and-click note creation, semi-structured “smart texts” which pull in data from the record, free-text typing, dictation – or even a mix of everything. As with most new roll-outs, our patient flow has been cut by 50% during the initial phase to cope with this learning curve. And I’ll freely admit that my first couple of appointments probably took about double the time I would have taken normally.
But let’s step back for a second. Really double the time? Really? What did I accomplish in that time? I completed my normal encounter (ignoring the computer except where necessary – I’m a patient-centered doc after all…) and then caught up with the software afterwards, transferring my scribbled notes into legible text and button toggles. I wrote my note. I wrote a prescription. I sent myself a reminder to call the family with the results of a lab test. I printed off a visit summary to give to the parents. Under the guidance of one of the “Super User” support staff I created a “new communication” to the kid’s pediatrician, linked my visit note, and faxed off a reply to the consultation. I selected a diagnosis and level of service, and with a click closed the encounter down.
I didn’t have to dictate a note.
I didn’t have to edit a note.
The pediatrician didn’t have to wait for me to dictate and edit a note – they had a copy of my recommendations at the office before the patient had left the building.
I didn’t have to flick through billing sheets, sign off on “problems lists” or “medication reconciliation logs”. I was all done with a click of a mouse.
It wasn’t extra time, it was reallocated time, time invested up front that saved me a ton of hassle later on. And as my learning curve moves up and I get faster at pulling down labs, creating smarttexts, macros and shortcuts this little beauty will truly save me time, AND provide better care for the patient.
Were there hiccups today? Of course, it’s a new system, but they had allocated sufficient personnel, expertise, resources and training into minimizing the problems and rapidly producing solutions.
A EMR is a tool – we still need our hands, our eyes, ears, stethoscopes and brains (and hearts…) to practice medicine effectively, but used properly something like this will only enhance what we can accomplish.
We entered a brave new world today, and I was the one to plant my feet in the sand before anyone else. It felt a little crunchy between the toes, but you know – I’ll have time to paddle in the surf later on.
The simple reason why I practice patient-centered care is that it’s better for the patient. But before I go into the details of that, we need to step back a bit.
Firstly, I’ll clarify what patient-centered care isn’t. It isn’t pandering to a patient’s or parent’s wishes and doing whatever they want, as a mere provider of healthcare. That is patient-LED care. I don’t think that’s always a good idea – most people after all have NOT gone through medical school and several years of practical training (something like 20,000 hours of supervised patient-care in my case) in order to make informed decisions on their health. Even though the Internet has leveled the information playing field considerably, you still have to know how to interpret that information in the appropriate context and with the correct background knowledge. There are places where patient-led care does play a role, but it is quite distinct from patient-centered care.
I define patient-centered care as “practicing medicine taking into account the patient’s concerns, expectations and understanding.” You may not find that definition anywhere else put quite like that, but to me it makes sense. It also follows a three-step process of “discover, validate, address” that I iterate through an encounter so that by the end we’re all on the same page.
When I was in medical school I was lucky enough to be asked to pilot a new curriculum element called Preparing for Patients (my sole legacy to Cambridge University is that I was the first to coin the abbreviation PfP – which obviously was no great intellectual feat, but I think worthy of a footnote in the annals of history). I was not yet seeing patients on the wards, and felt quite unprepared having spent much of my work experience during high school in various labs – examining things like different plant species, fiber glass tensile strength and drug purity.
PfP was an intensive program back then, a couple of weeks of daily sessions where we explored our own fears and thoughts on medicine and patients, then got to experience and practice actually talking to patients about their illnesses. The real beauty was in the use of standardized patients: actors and actresses who could give a consistent experience to everyone and respond to questions, even off-line, in character. I got to tell someone they had cancer with a 50% mortality several times before I actually HAD to tell someone they had cancer (which as it happens was at 2am one morning on call as an intern, by myself – that’s deserving of a blog post all for itself…). The experience was invaluable, and provided a toolset of behaviors, questions and actions (71 skills all told) that I could bring into play when I needed them during an encounter. I got to try out this new-fangled curriculum and provide feedback to the course creators on the process and content.
The course itself still stands, albeit in a greatly modified form. It is now a fully integrated part of the Cambridge curriculum, from the first year of pre-clinical science, and those 71 skills are the benchmark by which all Family Medicine (aka General Practice) docs in the UK are assessed for their board exams.
What I learned from that was invaluable – it turns out that talking to patients is a lot more than simply asking questions about their symptoms. Patients are people – they have preconceived ideas about their illness, they have worries, they have ideas on what needs to be done. Sometimes they’re wrong, in which case our job is to educate and reassure (or sometimes not…), but often they’re right and our job is to help get things done. I learned that illness (what a patient experiences) is different from disease (what a doctor treats). A tension headache is an awful illness, but a minor disease that the doc can do little about beyond over the counter pain meds. High blood pressure on the other hand usually has no symptoms whatsoever but serious effects on the body so that we want to treat it. The question was posed – how do you convince someone to treat something that isn’t making them sick right now?
What I also learned was that there was actually research to back up this approach – patient complaints and concerns about medical care (including well over half of all malpractice lawsuits) usually stem from communication failures or unresolved issues. Issues often were unresolved because the doc either didn’t allow the patient to bring it up, or didn’t explain things fully. Patients do not tend to bring up what medics would consider the most important issues first – for all sorts of reasons – and yet they are often cut off early in the rush to get them out the door and see the next one. Something as simple as asking “What are you concerned about?” early on in the encounter can save a ton of time, as you can focus in on what they’re most worried about right away. (Of note, you’ll get different answers asking that than if you ask “what are you worried about?”, which I find fascinating…) Making someone feel at ease is one way to encourage them to talk about embarrassing symptoms or scary possibilities, and there’s an entire skillset devoted to building rapport and trust for precisely this reason.
My general approach is the “discover, validate, address” thing I mentioned earlier. Discovering concerns may be as simple as asking them what they are, but there may also be subtle hints – a family history of cancer, a perseverance on a particular topic or symptom, facial expressions and other body language. You may focus in on something you notice, or use open-ended questions to hear things in their own words. It may be an ongoing process through the encounter, but ideally you get most of it done early on to avoid the “by the way Doc…” question as you’re wrapping up.
Validation isn’t simply agreeing with them – after all, people often get misled or misunderstand things. Validation is acknowledging that from their perspective what they’re feeling about something is entirely appropriate. They may be angry that their prior Doc didn’t treat symptom XYZ, but if, medically, it didn’t need treatment, then their Doc did nothing wrong. But if I can commiserate with them, ask about how it’s affecting their daily life, explain that this kind of symptom isn’t one we can treat – this often goes a long way to fixing the issue.
Addressing a concern may be already covered by just acknowledging its existence, but may require an explanation of why treatment or testing isn’t necessary, or it may require convincing someone to undergo a treatment plan that they’re really not all that keen on! It’s important to offer options – there is always the *option of doing nothing*, even though that’s not necessarily the best option. It’s critical to explain YOUR thinking about something – admit your biases, your own concerns about the patient – they’re more likely to follow through on your recommendations if they know why you’re sending them for blood work, x rays or a cardiac stress test – or asking them to pop a pill every day for the rest of their lives!
What this approach does is help the patient have more control over their medical care than an old-school paternalistic approach, but with more education and understanding than a patient-led approach. If you train doctors to talk to patients this way an amazing thing happens – the patients do better. Improved communication can improve management of diabetes and blood pressure, but also reduce followup visits and tests, lower reported pain levels, and some surprising things like reduced costs in the ICU. Others have already listed the main references. To me this proves two things.
Firstly – there are clearly deficits with doctor-patient communication that need to be and CAN BE addressed.
Secondly – YOU CAN TEACH COMMUNICATION SKILLS. I cannot overemphasize this enough. One of the largest myths in medicine is that you either have a good ‘bedside manner’ or you do not, and if you don’t you’re stuck with it. That simply isn’t true. You CAN teach medics of all levels – from medical students to consultants – new skills and demonstrate changes not just in their behavior, but in their PATIENTS’ behaviors. This is an astonishing finding, and the skills can persist for years. The only thing more astonishing than this finding is that we’ve known about it for decades. Communication skills are being given greater emphasis in medical school these days, finally, but testing is haphazard and unhelpful a lot of the time (feedback 3 weeks after a standardized encounter is nowhere near as helpful as an immediate conversation and a chance to do-over the visit) and training is often limited to lectures rather than structured practice sessions. It is difficult to teach it properly, and it is certainly difficult in an area traditionally taught through lecture format, and which is increasingly moving towards online self-directed educational formats. Carving out a 1-2 hour block of time every week to sit down in small groups with a trained facilitator and one or two trained standardized patients is what’s probably necessary, but I doubt many course organizers think that they’re able to do that – my argument would be that we need to find a way to make it happen, not that we avoid trying because it’s difficult. I am living proof that you can take someone who honestly was pretty socially inept and turn them into someone who can not only practice patient-centered care, but teach it to others. Throughout my residency and fellowship I led a group of child-life specialists, Residents and Attendings in weekly sessions with the pediatric clerkship students teaching a modification of the Calgary Cambridge Guide.
One common criticism about teaching patient centered care or communication skills is that it somehow detracts from the teaching of “real” medicine – the mass of signs, symptoms, risk factors, tests and treatment options that we basically have to rote memorize, as well as the practical application of all that knowledge with real, sick patients. My counter to that is: who says the two are mutually exclusive? You can learn medical facts during the practice sessions, you don’t need to know them beforehand. You can integrate the two aspects of medicine – and in fact you probably need to integrate them or else risk maintaining the mental block between “real” medicine and “communication skills”. Real medicine relies on communication skills to elicit a history and convey a plan – how else do you think this can be achieved? Telepathy? Flash cards? Who says you can’t run a code in a simulation then afterwards have the “breaking bad news” simulation with the manikin’s “relatives”?
And finally, doctors that have a disease-focused approach are more likely to experience patients as “difficult”, and those patients are more likely to have additional (unnecessary?) visits, than if the doctor had a more patient-centered approach. Patient-centered docs are happier docs.
So, to me, effective communication skills are an absolutely integral aspect of patient-centered care, and patient-centered care is a way to dramatically improve patient outcomes. These skills can be taught, and I argue they should be taught if we truly want the best for our patients.
If any readers of this actually do rotate through ID with me, remind me to discuss the process of an encounter as much as the content…I tend to forget!
For those who haven’t been under a rock recently, several parts of the US have seen a surge in pertussis cases. Much of this has been (fairly) blamed on anti-vaccination efforts to reduce herd immunity and the cocooning of vulnerable infants. But that’s not the whole story.
Interestingly enough, it’s now clear that the DTaP vaccine (diphtheria, tetanus, acellular pertussis) doesn’t provide long-lasting immunity. We had some clues with this as an awareness grew of pertussis in older teens and adults, fueled in part by vastly improved testing for pertussis (PCR versus ‘cough plates’ for culture) and a recognition that pertussis in older kids and adults didn’t look like the classic ‘whopping cough’ that youngsters got.
A booster dose of pertussis vaccine was recommended, included as part of the tetanus booster (the new Tdap vaccines). Recent outbreaks seemed to focus on the group of kids aged 10-11 years of age – when vaccine immunity was waning, but just before their Tdap booster – but the recent outbreak in Washington State has involved even 13-14 year olds, who did get their booster!
The question then should be – why does the NEW vaccine work LESS well? The answer is because it is SAFER.
The old DTP vaccine began to get a bad reputation for neurologic disease – in fact a contraindication still exists to withhold pertussis-containing vaccines in kids who develop neurologic issues after pertussis vaccination, even though the vaccine is different. The old DTP contain literally thousands of antigens, based as it was on a relatively impure cocktail of cell culture fragments that contained the pertussis bacteria. It caused a fair amount of immune reaction, and clearly was linked to febrile seizures.
Several high-profile cases of apparently neurologically damaged children (leading to the formation of some of the early modern anti-vaccine movement) pushed the vaccine manufacturers to create a cleaner vaccine, an ‘acellular’ pertussis vaccine, which is why we have DTP and DTaP. DTaP doesn’t have the same link of febrile seizures and no link to any neurologic issues (interestingly, as detailed in Paul Offit’s book on the history of antivaccine junk science, neither do any of the original DTP kids…it was all a big screwup). Tdap is even less immunogenic as it has slower concentration of antigens – you can tell this because it has a small “p” instead of a big “P”. True story.
The trouble of course is that by having a less inflammatory response, with far fewer antigens, the protection is less. The original DTP vaccine contained more antigens than the ENTIRE modern vaccine schedule does, several times over. Any statement about ‘too many too soon’ is pure bunk – our kids are exposed to fewer vaccine antigens in their entire schedule that we were in one vaccine.
This story highlights several points – firstly, contrary to antivax propaganda, not only are there mechanisms in place to detect and respond to potential vaccine side effects but there are CHANGES made to the vaccines in an attempt to keep people safe. (Probably the only positive thing to come out of the antivax movement is the establishment of the Vaccine Adverse Event Reporting System, VAERS). Secondly, there are compromises to be made – more effective sometimes also means more side effects, so if you want to lower one you may end up lowering the other.
There is also data from Europe that as the vaccine strains of pertussis wane, there is strain replacement with potentially more virulent strains. So although we are seeing fewer cases, those cases we do see may be more serious (this finding hasn’t yet held true for the US…as far as I know).
Of course the antivax brigade have twisted the story yet again “Whooping Cough Epidemic Caused by Virulent New Pertussis Strain—And It’s the Result of Vaccine” shouted one headline. While technically true it doesn’t really go into the real explanation of WHY…even more impressive, but entirely unsurprisingly to me, the actual article the antivax site uses to support their claim starts with the words “Before childhood vaccination was introduced in the 1940s, pertussis was a major cause of infant death world- wide. Widespread vaccination of children succeeded in reducing illness and death.” which not only proves how disingenuous antivax proponents are, but how stupid they are. The first rule of selective quotation is to use sources that support your argument.
Sadly, those who believe antivax propaganda are not usually stupid – if anything they tend to be more educated than average, and well read. They just read the wrong things. Not everyone can go to medical school after all.
Then again, even that isn’t foolproof. One of the original antivax “Expert” witnesses from the UK trials that showed the DTP link with neurologic illness to be wrong went on to further his infamy with AIDS denialism.
Much of the details on the stories of the DTP and DTaP history are in Paul Offit’s book – Deadly Choices, which I highly recommend. In it he not only details how antivax proponents twist science and the facts to suit their case, but also how they nearly brought down the entire US vaccine industry through irresponsible and indefensible litigation. The vaccine WORKS to reduce serious illness from pertussis and undoubtedly saves lives. It’s not perfect, no one has ever said a vaccine was perfect – at least, not unless they were trying to make a point that it wasn’t…
“No maternal history of herpes”
When dealing with a newborn baby with a fever, those are words that strike fear into my heart.
Wait, what? You said no maternal history? Yep, that’s right.
Neonatal herpes simplex virus (HSV) is a topic that is full of counterintuitive statements, and far too much confusion. The wrong people get tested, the wrong people get treated, the wrong babies get worked up aggressively. When other docs diligently rattle off the “pertinent” aspects of the maternal history and clinical examination of the baby, in my mind I’m mostly saying “Don’t care, don’t care, don’t care….” before I interject and ask about test results that often haven’t been ordered.
Based purely on a numbers game, thanks to things like vaccination and Group B Strep prophylaxis, many early onset infections in newborns have been reduced. There is simply less infectious disease hanging around. But as a result, viral infections like neonatal herpes are proportionately becoming larger players – in some hospitals it is as common as bacterial meningitis. And neonatal HSV is a killer.
HSV comes in three distinct flavors – the least lethal is skin-eye-mucus membrane (SEM) disease. This is how many people expect to see herpes – a rash, typically vesicular (clear fluid-filled little blebs) and maybe some eye discharge or mouth sores. Most pediatricians, if they see something like this, appropriately freak out a little bit. SEM disease by itself isn’t too dangerous, and if treated properly is almost never fatal. Herpes is tricky though – in babies it can mimic other rashes, so you really do need a low threshold to consider it. ANY neonatal rash that doesn’t fit a normal neonatal rash (so know your neonatal rashes!) deserves a workup. There is nothing more sobering than to run a case of a neonatal rash by an ID doc and to have them tell you with complete sincerity that “You can save this baby’s life. Get them to an ER. Now.” Untreated SEM disease can progress to infection of the brain.
The most obvious presentation is disseminated disease – which weirdly enough can occur before SEM disease…first week of life or so. The kids are sick – really sick. They can be in shock, bleeding, in liver failure and struggling to breath as the virus overwhelms pretty much every organ system. The problem here is that even faced with this situation bacterial infection is considered immediately, and herpes can still be overlooked or thrown into the mix as an afterthought. Again, good neonatologists and pediatricians will be all over this from the start, having experienced their share of disasters in the past. Disseminated herpes is mostly fatal without treatment – and even with therapy about a third will still die, many of the survivors left with significant disabilities.
The last type of herpes infection is of the brain. Typically presenting later in the neonatal period (3-4 weeks of age, rarely later) herpes encephalitis of the newborn is devastating. Herpes causes a hemorrhagic encephalitis, meaning that it chews your neurons up into a bloody pulp. To a brain that has barely begun its developmental process, this is a disaster. Even if the baby survives they may be blind, deaf, paralyzed or have significant developmental delays.
From how I describe it above you might assume it would be easy to spot these kids. Well, it is – once it’s too late. The success of treating HSV depends to a large extent on how quickly you can start acyclovir – one of the few medicines we have that can treat viral infections (it’s pretty much only used for HSV). Acyclovir can shut down virus replication, but does nothing for those cells already infected. The difficulty with HSV lies in the nuances of the medical history.
Let’s try some armchair science for a bit. Would you, as a baby, rather get HSV from a mother who is having a recurrent outbreak of HSV, with low-levels of virus, and have her give you antibody protection through the placenta…or would you prefer to catch HSV from a mother who is having her FIRST outbreak (which may be without symptoms) with high-levels of virus and no antibody protection? Well, you may ask, how likely is that? The answer is Very. About 90% of all neonatal HSV cases come from mothers with no history of HSV. If your mom DOES have HSV and has a recurrent outbreak, the risk of transmission is about 5%. For a new case – its closer to 50%. Maternal history of HSV is relatively PROTECTIVE for the baby.
But the focus is on the mothers who test positive for HSV during pregnancy. They get put on valtrex (an oral version of acyclovir which is well absorbed), when it has not been shown to sufficiently reduce transmission. They may get a C-section, when that hasn’t been shown to help either (except maybe in the case of active lesions at the time of delivery…and even then it’s unreliable). The mothers who are HSV-negative are ignored, when they are those at highest risk of passing HSV to their babies. In an ideal world, their sexual partners should be tested and if THEY are positive THEY should be put on valtrex to reduce outbreaks and educated about the risks. But the fathers aren’t the patient….so nobody does that.
A big myth about HSV is that all babies with it look sick. Well, they do eventually – but to start with they look pretty normal. I have heard docs say that a baby looked “too good to tap” – meaning they didn’t perform a spinal tap to check for meningitis or HSV encephalitis. Or they don’t test sufficiently for HSV, or don’t start treatment with acyclovir while test results come back (these same babies are almost universally started on antibiotics for presumed bacterial infection). Published case series of proven HSV cases shown over and over again that babies with HSV present with relatively innocuous symptoms. “poor feeding” “fever” “sleepiness” before the more obvious symptoms of “shock” “seizure” or “respiratory distress”. Remember, by the time the baby is sick from HSV the damage has already been done, and you can only try to stop it from getting worse and hope the kid recovers. With bacterial infections we can kill them directly with antibiotics and the damage is usually secondary to the infection, and not because the bacteria are literally eating up your cells and blowing them apart as HSV does. Even with successful treatment, symptomatic HSV in babies has a slow recovery.
So how do you deal with this uncertainty? You can’t trust the mothers history, you can’t trust the baby’s physical examination or symptoms…what do you do?
My approach is to have a low threshold for suspecting HSV in neonates. ANY baby getting worked up for a possible bacterial infection needs to have a workup and empiric treatment for HSV as well. Babies with weird symptoms (especially rashes or neurologic symptoms) need to have HSV considered FIRST, before bacterial causes. HSV is not only potentially devastating – its treatable, and therefore the bad outcomes are preventable.
Fortunately the Committee of Infectious Diseases of the American Academy of Pediatrics has published recommendations – albeit in a rather inaccessible set of paragraphs. I can summarize them here though:
Spinal tap for HSV PCR of spinal fluid.
Liver enzyme testing for disseminated disease – chest x ray if respiratory symptoms.
Surface cultures from eye, mouth, rectum and any skin lesions.
Start acyclovir – do not stop until all tests are negative.
Do ALL of this this for EVERY BABY with suspected HSV.
Repeat spinal tap on kids with positive CSF to ensure clearance after 21 days – continue therapy if still positive.
A big mistake I see people making is in testing the spinal fluid to “rule out HSV” but do not doing the rest of the workup. Spinal fluid testing for HSV no more rules out SEM or disseminated disease than a urine culture can diagnose meningitis. I have seen cases missed (or nearly missed) because someone didn’t do the whole thing. You NEED the liver enzyme testing to rule out disseminated disease, and it matters. Treatment for simple SEM is 14 days – treatment for disseminated or CSF disease is 21 days. I have seen a handful of kids with positive CSF tests but with totally normal looking spinal fluid (eg no white cells, normal protein levels etc).
The trouble is HSV, as bad as it is, isn’t all that common among the hundreds of kids you will see with suspected neonatal infection. And many of THEM will be obviously HSV. So many kids get a semi-workup and we get away with it because “whoops, the CSF is positive!” and you treat for 21 days even though you didn’t check the liver enzymes.
But I’ve also seen the opposite – kids who were partially worked up and the diagnosis was missed, or delayed, or the severity was under-appreciated. All too often the “standard of care” let’s these kids slip through the cracks – which is inexcusable in my mind when there are experts who put it down in writing exactly how to work up these cases.
So let’s raise the standard.
Totally useless history:
Mom has no history of HSV
Mom got Valtrex
Mom got a C-section
Baby looks well
REAL risk factors for neonatal HSV:
Prolonged rupture of membranes
Active lesions at time of delivery
NO maternal history of HSV
Age less than 21 days
Seizures or lethargy
“Sepsis” not responding to antibiotics (oops! too late! – better call your lawyer…)
PCR/Culture of skin lesions, eyes, mouth, rectum
Liver enzyme testing
Chest X ray (if symptomatic)
Acyclovir 20mg/kg/dose IV every 8 hours
Until all tests are negative (typically 2-3 days empirically)
14 days for proven SEM disease
21 days for disseminated or CNS disease
And if you’re not sure…get a consult…