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…
As a consultant my expertise is sought out in largely two ways – a formal consultation (a request to see a patient, obtain a history and perform a physical examination, review laboratory tests and recommend further evaluation or treatment), or a curbside question (a quick hypothetical or general question with the expectation of a simple answer).
An example of a curbside question might be “How many pneumococcal serotype responses would you expect to be normal in an immune evaluation..?”. The answer is 5-10 depending on the age and immunization status of the child, but in reality the correct response is “why the heck are you ordering an immune evaluation on a kid that I know nothing about…?”. The indications for performing an immune evaluation (frequent or unusual infections) are generally the sort of thing an Infectious Disease specialist should have been consulted on!
People often start a curbside question with “This isn’t a consult, but…” as if a consult is a bad thing. It isn’t. A consultation isn’t an inconvenience, it’s what I get paid to do (salaried or not, divisional revenues ARE based on the consults I get called to see). It’s what I ENJOY doing – if it wasn’t I wouldn’t be in the job in the first place. And even if I AM busy, tied up in clinic, or off-site taking call from home, it’s in the patient’s best interest.
No matter how well you quiz someone over the phone, there is no way they can adequately convey the entire medical history and physical exam, the concerns of the patient and family, trends in lab values, recent antibiotics and other meds, and the simple gut vibe of a case… A complete consult, done properly, can take up to an hour and may involve field trips to radiology and the micro lab to check things out for yourself. That is a considerable chunk of time (certainly more than a curbside question) but the value of having a subspecialist see the whole picture cannot be overstated.
The dangers of answering a curbside about a specific patient are legion – you may miss drug allergies or interactions, co-existing diseases or subtle clues in the history or exam that would point towards a specific diagnosis, you will tend to overtreat “just in case”, lacking the reassurance of seeing the patient for yourself, but may just as easily undertreat an infection that had been missed or misdiagnosed. Worse, for the consultant, chances are good that their name will end up in the chart “case discussed with ID”, which medico-legally puts us in a bit of a spot. Then the onus is on you to show that you had no medical obligation or responsibility to the patient should something bad happen…a hassle and horrific waste of time at best.
The other issue is “added value”. Even when I’m called to answer a specific question, I almost always end up offering something else. If I’m asked about best treatment options, I will offer alternative diagnoses. If the question is what this disease could be, I will recommend empiric therapy as well. Every consult is a teaching opportunity, whether about a specific disease or a general bit of advice on ID. For THAT patient I want the docs who consult me to know as much about the disease as I do.
That’s all in theory – what about the evidence? One study of mandatory ID consultation for outpatient IV antibiotic therapy found that 39 of 44 patients had a change of therapy (!), meaning that 88% of the time the current plan was not ideal. 39% of the patients were sent home on oral instead of IV antibiotics, 13 patients (30%) changed medications, 5 patients changed dose, 3 changed planned duration, and 1 patient was stopped entirely. Cost savings were $500 per patient EVEN TAKING INTO ACCOUNT THE CONSULT FEE. In Germany and the US, ID consults have been linked to significantly reduced mortality from staph infections. In Italy, formal ID consultation on ICU patients reduced cost, mortality, ICU stay, length of mechanical ventilation – all due to improvements in antibiotic usage. A financial analysis of curbside consultations suggested that close to $94,000 in revenues were lost in a year by giving advice over the phone without performing (and billing for) an appropriate level of consult. With antibiotic cost savings and increased revenues to the hospital, consults really are a win/win situation.
So what’s really happening when you say “This isn’t a consult, but…”? You’re putting your patient at risk of being treated for the wrong diagnosis, or being wrongly treated for the right diagnosis, you’re increasing hospital costs and increasing patient mortality, and you’re passing up the opportunity to learn something yourself. It’s not good medicine – it’s not good for anyone.
Say it after me: “I’ve got a consult for you…”
This post may or may not have been inspired by the fact that I have had an inordinate number of consults this week which started out as curbsides that would have led to inappropriate care….
I was recently asked “what is a line infection?” and I realized that it would take more than 140 characters to explain everything about it. I also figured it would be a good topic to educate on, since as a whole line infections are very badly managed.
Briefly, a line infection refers to a bacterial (or fungal) infection of a central line, usually in a vein but an arterial line could get infected too. The classic case is a catheter tip infection with bacteria in the bloodstream. The patient may have a fever, and may be quite sick indeed.
One might ask; “How the heck does that happen??!!”. Actually, surprisingly easily.
Lines can be infected from two ends – the outside end is open to the air and is accessed every time a medication or IV nutrition is put through it. If sterile technique is not used bacteria can get into the line. Heck, even with sterile technique bad luck plays a part too. These bugs are often skin bacteria that are normally fairly wimpy or considered “contaminants” when grown in blood cultures (meaning they were picked up from the skin as the needle went in, not that the lab contaminated them!). The inner end is safely inside a blood vessel, which is sterile, but if bacteria get into the bloodstream for other reasons they can stick to the plastic line, since bacteria as a rule LURVE to stick to non-biologic stuff. These can be any kind of bug, but are more likely to be bacteria from the gut who wandered off accidentally in the bloodstream and find a home there before the immune system can kill them off.
Once a line infection is established, we have a problem. Plastic lines have no bloodstream and no immune system. Bacteria can produce slimely stuff (called a biofilm) that coats the infection and acts as a barrier to the immune system, and some antibiotics. Imagine smearing peanut butter on a table, then trying to get it off with your finger. Even after a good swipe you’ll leave a smear behind. Now imagine trying to clean it off by dripping detergent onto it. That’s what it’s like trying to clear a line of a line infection. The only way to guarantee clearing a line is to pull it out and put a new one in.
Pulling a line is not a lightly-undertaken job though. If someone has a line they probably have a reason for it – long-term nutrition, chemotherapy, antibiotics etc. If you pull that line you may interrupt their usual doses, for days at a time. Line sites get scarred and if you do this enough you can run out of new sites to use! So it’s paramount to diagnose a line infection properly.
Imagine the following: a kid with a line gets a fever. They come to the hospital and blood cultures are drawn from the line. They grow a staph aureus. OH NO! He has a staph aureus line infection right? Not necessarily. Blood drawn from the line is just blood – this could be any other staph bacterial bloodstream infection, such as from a bone or joint infection, endocarditis (infection in the heart) or something else. We need to know whether the line has more bacteria than the rest of the blood stream.
This is where most people go wrong – you MUST MUST MUST draw multiple cultures, including a culture from some place else (and yes, this means sticking a needle in someone – suck it up). Ideally you need quantitative cultures, where you draw a fixed volume of blood then plate it out and count the colonies. If the line cultures grow significantly more than the periphery, it’s a line infection. If it’s the same, it is a bacterial bloodstream infection, but not a line infection. BIG difference. If you can’t do “quants” you can time how long the cultures take to turn positive in the lab. Most experts consider a difference of a few hours to be significant.
Once you know it is a line infection, you can think about what you’re doing. Most people get started on broad-spectrum antibiotics to cover all the likely bacteria. Once you know your bug though, you can tailor therapy. Non-Aureus staph for example may actually be cleared using a couple of weeks of antibiotics. Enterococcus or staph aureus are tougher, gram-negative bacteria from the gut are even worse. Pseudomonas or candida/other fungi are practically impossible to clear, don’t even try.
What’s the harm in trying? Time. You waste time. You have a kid sitting in the hospital getting IV antibiotics. You may send them home…and you may be able to show that the blood cultures turn negative….but you stop those antibiotics and WHAM the peanut butter smear you didn’t quite clean off has grown back into a big old dollop of yuck again. You’ve wasted 2 weeks at least, several days of hospital time AND now you’re back at square one and you have to pull the line you should have pulled two weeks ago.
The two biggest errors I see people try with line infections are: not correctly testing for line infection with sufficient blood cultures; trying to salvage an unsalvageable line. People are fooled into thinking they have cleared a line infection, when in fact they may have been treating a bacteremia from another source and just THOUGHT they were treating a line infection. This reinforces the incorrect belief that clearing line infections is easy…
I get consulted on these kids. I can rarely offer specific guidance unless the correct workup has been done. I have seen kids get lines out that I am sure were not infected, and I have seen kids treated for weeks for an infection that could have been cured with a 30 minute procedure to pull the line out. There are evidenced-based guidelines on this issue published by the Infectious Disease Society of America – ID docs KNOW how to manage line infections – and yet our guidelines, and our specific advice, is often ignored.
Best reason I was ever given for not removing an infected line? “We can’t take it out, we’re using it for the dopamine”. Yeah, well maybe if you stopped using it the patient wouldn’t be in shock any more…
Incredibly, since I have been in my new position for over 6 months, this morning was my first lecture (but I use the term loosely) to the residents here. It was ostensibly on “infectious rashes and infestations” – but I entitled it “Nasty skin infections – cos there really aren’t any nice ones”.
It was apparently well received.
I have a knack for teaching. I’m not saying that because I think I have a knack – other people have told me so. I have various awards to show for it. I have people ask me to teach, and I assume it’s not just to hear my awesome accent. It has a history going back to high-school where my friends would ask for help with their homework. I had the annoying habit of not giving them the answers – rather I would try to help them figure it out for themselves – responding to their questions with questions of my own. I don’t remember whether I did this out of a sense of mentorship – the benign guidance of a sage helping them to reach their potential – or out of sheer bloody-mindedness and for my own amusement. I do know I simply didn’t think it was “fair” that I had to figure it out for myself but they wanted the answer simply given to them. I can’t blame them – we all want that at some point.
In medical school I found myself struggling in a competitive, highly academic and esoteric system which I was pretty unprepared for. I remember writing a scathing review of the teaching I had received there for my college magazine. I “dropped out” of one tutorial class to do self-study instead, and brought my grade up two points as a result (on a 4 point scale, that’s not bad…). I laid down the mental framework for how I wanted to be taught, and applied that to others where I could. I was lucky to be asked to supervise (teach, in Cambridge lingo) genetics and virology to two of the university colleges for two years. Ironically I found myself as a flawed part of the very system I had complained about – flawed in that I was teaching without any training in how to teach!
It was in my residency however where I really found a role for myself in teaching. My wife tells me that I “like telling people how it is”. She may be right. In any case, there are ample opportunities for teaching medical students, junior residents, peers and colleagues during the years that you yourself are getting educated and trained in medicine. I developed my own style – honed through trial and error, practice and observation. My research years had taught me a lot about how to teach and how NOT to teach effectively – and also removed whatever fears of public speaking I might have harbored. We all know that “teachers teach how they were taught, not how they were taught to teach”, but I made a conscious effort to TRY to teach using techniques that I knew to be effective, even if I hadn’t experienced them directly. I cherry-picked those I liked and adapted them to my own personality.
The techniques weren’t all that became developed – my repertoire of content grew and was refined. For most of the topics I was asked to teach about I got to the point where I could grab a pen and paper, or whiteboard, and put together an interactive case-based 1-hour teaching session with no notice.
After today’s success I thought a little about my role as a medical educator, and I remembered something.
Doctor. We all know what it means. Or do we?
It means “Teacher“.
The word “Doctor” has been hijacked by the medical profession (and other related careers), where in fact it was intended to mean someone with sufficient learning in a subject area to teach others. Technically in fact, most medical degrees aren’t “Doctorate” level at all, since they are “first degrees” in medicine, regardless of whatever degrees a person may have in another subject. My own medical degree reflects that: MBBChir, Medicinae Baccalaureus, Baccalaureus Chirurgiae – Bachelor of Medicine, Bachelor of Surgery. An MD in the UK (and almost everywhere except the US) is a true post-graduate degree with a research dissertation.
Ironically the medical profession seems to have forgotten that. Medical education in the US is an oft-neglected role, poorly reimbursed, run by those with a passion for teaching while feeding off the table scraps that their procedure-driven peers feed to them through the teaching hospital income. Until recently, there were few real incentives to teach or contribute to medical education – promotion and bonuses were linked to clinical revenues and research grant dollars. I am fortunate to work in one of the (apparently) few places that does place a value on medical education such that I can use it for career advancement rather than a hobby in my spare time. People go into medicine for all sorts of reasons – to help people, to heal, to make money, to do cool procedures and surgeries – but I doubt very many go into medicine to teach.
And yet they carry the title of “Teacher”. My own career track is that of a “medical educator” – which seems to me to be a redundant phrase, if you think about it. The fact that we have to label medical educators as something special shows how we have drifted away from the true meaning of “Doctor”.
To go back to our roots, we should ALL be educators. Every year there is a wave of students leaving their education and entering training, and a wave of residents leaving training and entering the real world. These men and women need guidance. Beyond the academics and pearls of wisdom, they need mentoring, career and business advice, insight into work-life balance and their options beyond the ivory towers. They need to know how to recognize meningococcemia, but they also need to know how to get a parent to recognize it over the telephone. They need to know when to admit a patient, but also how to bill for that admission. They need to know how to convince a skeptical teenager of a treatment plan, and how to negotiate a partnership contract.
Physicians don’t have to work at a medical school to teach – they can contribute to career fairs, social media, newsletters, take on elective students in their practice…anything is possible. There are literally hundreds of thousands of years’ of experience out there waiting to be tapped…
So I urge my medical colleagues – reflect on this. Remember your title, your role in history and the potential you have for leaving a legacy of medical practice in your wake, in the form of the next generation of Medical Doctors.
As Hippocrates himself said:
“…I will impart a knowledge of this art to my own sons, and to my teacher’s sons, and to disciples bound by an indenture and oath according to the medical laws…”