Archive for category Guidelines
I saw a very disheartening quote in a patient chart recently:
“…consider curbsiding ID for antibiotic recommendations…” Followed a few pages later by “Follow ID recs…”
It was disheartening in several ways: firstly that although someone had obviously thought us worthy of asking for advice they hadn’t actually called me about the patient; and secondly that they thought this question was worthy only of a “curbside”.
Regular readers and followers will already know my thoughts on curbsides – but I didn’t really delineate what I actually do. I addition, what should I expect of a consult and what should a consulter expect of the consultant?
A consult is triggered, at least on the inpatient side, when a physician asks a question of a colleague in another speciality. Now this happens informally all the time – we live in a learning environment after all – but a question along the lines of “I have a patient…” generally means that there are healthcare decisions being made on a real patient, and these are the real issue.
Most of the time a consult requires a specific question – I have had colleagues in fact pause for thought and tell me “I’m not really sure what question I have for you…” and then not bother formally consulting. In my mind, it’s very simple – if you are concerned or uncertain enough to seek out a subspecialty colleague for advice on a specific patient, that by itself is valid grounds for a consult. I have done more than my share of consults for “please assist with antibiotic management or further workup”. It’s not failure or weakness, nor a waste of my time – it’s what I do and it’s in the best interests of the patient.
I do expect a somewhat valid reason – a specific question is ideal, but even if I’m asked about antibiotic treatment I will usually try to go beyond that and include alternative diagnoses, testing, followup recommendations etc. I also expect timeliness – a consult should be called early, both early in the disease course and early in the day! I prefer to avoid problems than have to dig people out of them. I also like time to go to the lab before seeing the patient…and recently I had to fish culture plates out of the trash in order to help a colleague with antibiotic recommendations. Had they waited another day we would have had to use unnecessary antibiotics to treat more broadly than we needed to. Calling a consult prior to knowing all the information is ideal – I can often get preliminary results faster than the lab will report them and add on additional workup days ahead of time.
When I get asked a “simple” question like what antibiotics are recommended I go through the following steps:
Initial shoot-from-the-hip thoughts – what info do we have so far? How sick is this kid, risk factors, early lab results and prelim microbiology workup. I will ask for CBC (with diff, always with diff), CRP and sometimes ESR, renal and hepatic function as appropriate. Urinalysis results, and CSF findings if an LP was done. Empiric bugs will depend on likely source of infection and likely site of infection – the two might be quite different! Then I ask what drugs the kid is on and line up the likely antimicrobial activity of those drugs against the likely bugs and see if there are holes in coverage. I do this last step mentally over the course of a few seconds (usually) but I do it every time. Typically when I do the same process with residents or students it’s a several-minute slog through the bug/drug matchup table. Just because it’s easy for me doesn’t make it worthless though, it just makes me efficient. If the kid is “safe” then I tell them to stay put, if not I suggest additional empiric coverage before I even see the patient.
Second stage – chart review. I read the chart. Yeah, I really try to read it. ER records, admission note, progress notes, operative notes and even resident signout notes… I will scroll through every lab in the computer even if I don’t transcribe every one into the chart. Every microbiology lab, positive, negative or pending is recorded. I personally looks at x rays, scans, even ultrasounds (although my ability to read those things is pretty near useless). I always review the scans myself and THEN read the radiology report. Sometimes I’ll go down to radiology and review it with the radiologist.
At this stage if there are questions or additional workup obviously needed I will call the lab or let the team know, and if I get the chance I will physically walk over to the lab to look at the cultures myself. What’s the value in that you might ask? Well more than once has an initial “gram positive” gram stain turned out to be a gram-negative bug, and in some cases a gram stain alone can, with the right eyes and expertise, result in a diagnosis all by itself. On the culture plates, bugs like proteus, klebsiella, strep viridans, listeria, E. coli and pseudomonas have a characteristic appearance (and smell!) that may jump start the management a day before the Microscan or Vitek machine gives you the formal identification. A visual peek at a urine plate reported out as “flora” might reveal a predominant organism that you can point to and ask to get worked up.
Lastly – the patient. Go to the bedside, lay on eyes and hands. Talk to the parents and patient and find out the little nuances in the story that others missed – the dog bite in a kid with fever, the recent dental visit in a kid with bacteremia, the rash in a mom that started the day after delivering her baby… Test hypotheses, confirm or refute suspicions.
Sometimes with all of this I rethink my initial plan – which only goes to show how unreliable the shoot-from-the-hip curbside is. I may back off from my broad empiric coverage, or I may rethink a diagnosis completely and expand both therapy and workup. It’s not unusual for me to be consulted on disease X and have to tell the team that it’s really disease Y all along. A curbside cannot possibly do that. Any result requires a conversation with residents, students, nurses and colleagues – all of it educational and a two-way process.
So if you add all this up, what does it mean? It usually means, at minimum, a level four inpatient consult. Consults come in five levels – short of a life-threatening condition this is about as high as you can realistically go.
Let that sink in for a bit. A simple question of “what antibiotic should I use?” is justifiably as difficult as a decision to do elective surgery. In fact, based purely on asking me to review the evidence running up to the decision, there’s enough work to bill at that level even if I say “you’re doing a fine job, I recommend no changes or further workup”.
Yes, Infectious Disease specialists do all sort of other cool stuff too – we diagnose rare diseases, can help with resistant organisms or diagnostic dilemmas – but fundamentally we’re trained in how to best manage all the routine stuff as well. That’s not to say we need to get called on every pneumonia, meningitis or urinary tract infection – but if you get stuck with a question or concern with any of these it’s ok to ask for help.
And if you’re going to ask for help, don’t, just don’t, assume it’s not worth anything. No-one would dare ask a surgeon to operate for free…why treat your ID colleagues any differently?
“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…
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…