Friday, October 21, 2011
People should be admitted to the hospital because they are sick enough to have an increased chance of dying relative to those going home. My overall patient-by-patient "mission statement" is: Find the diagnoses and offer treatment options that decrease acute mortality and chronic morbidity through efficient and high quality care. Offer palliative care options when such treatment is medically futile or does not provide significant gains in the quantity to quality of life balance. The patient needs to be looked at as a gestalt of both data and intuition regarding the level of acute injury inflicted on the substrate of a certain level of chronically damaged protoplasm. I have to explain to my patient and their circle that based on what I think is going on, will the treatment options available improve their lives and do those benefits outweigh the risks of that treatment. If not, pursuing aggressive treatment of the untreatable is a study in futility, and palliative care options should be introduced. Understanding the worst case scenarios, is in my opinion, more valuable to both provider and patient than painting a rosy picture of the future. It is important to foresee negative outcomes to know what to test for and what you may need to treat, but without either you or the patient losing sight or hope of positive outcomes. Positive outcomes do not necessarily mean a cure, it may mean pain control, dignity, and even a peaceful death.
Sweat the Details
A good internist is a scared internist. Worried about what has happened, concerned about why the current state of their patient is different from before, wondering how complications can occur in the future. We take a microscope to abnormalities, trying to tease out if this is incidentally benign or malignant, wondering if this is evidence of disease or simply a normal perturbation. Hospitalists must be the diagnostic laser, making lightspeed decisions about what to pursue and what to defer as well as carefully convey to outpatient follow-up. We must carefully dissect subjective complaints and objective data using the scalpel of evidence-based criteria and a wealth of subspecialty guidelines. We must thin the electronic medical record of redundant or inaccurate diagnoses while updating it with new history. The patient's medication list is not simply the medications they are prescribed but those they are actually taking and when they are taking them. A hospitalized patient demands an agent, their hospitalist, who manages nutrition, hydration, electrolytes, medications, and ancillary therapist evaluations while requesting appropriate specialist consultation and preventing adverse events such as deep vein thrombosis, falls, and delirium. We must take a collection of prior documentation to weave a history, amalgamate in-patient events, tests, and consults as daily progress notes, and then meticulously sift all of this into a timely, complete discharge summary.
Achieving Hemodynamic Homeostasis
I consider vitals to be an acronym for Verify If They Are Living Still. In general most hemodynamically regular people are euthermic with a heart rate between 60 and 90 beats per minute, breathing 8-16 times per minute, have a systolic blood pressure greater than 100 mmHg and less than 160 mmHg, and saturate greater 92% on room air. If they don't they are either (1) acutely sick with a physiological response, (2) chronically sick and at their (albeit abnormal for the majority of the human population) baseline, or (3) weird. Acutely ill humans should have a positive response to appropriate therapy, that is there vital signs approach normal, and negative one to inappropriate therapy. That being said, people die even despite the most optimal of treatment decisions, and people live despite our best unintentional attempts at killing them. You have to determine whether the population mean abnormal vital sign(s) are an indicator of acute pathology or simply evidence of chronic but stable disease.
Returning the Patient to Basal Levels Lab Result Rubor
People are often admitted because of the density of red (abnormal) test results they have. Although abnormals should be recognized they should also be placed within the context of their chronicity and severity. Some patients have bloody diagnostic tests at baseline. An elevated white blood cell count can be due to chronic lymphocytic leukemia, dehydration, stress, or infection. No matter what we as physicians do, it is unlikely that no matter what we do acutely we cannot change the leukocytosis of CLL. Antibiotics do not treat dehydration or stress, but not treating a pneumonia with its associated leukocytosis is tantamount to medical crime. Similarly a volume depleted patient may have a CBC in the black, volume contraction hiding their basal anemia, just because they are less in the red, doesn't mean they are any less sick. An elevated creatine in a patient on dialysis has an impressive crimson hue but generates little therapeutic inertia compared to the same value in someone without previous kidney disease. No matter what intervention is undertaken, the patient with end-stage renal disease will never be in the black when it comes to creatinine, if we waited for this value to normalize before discharging the patient, they would serve a life sentence. As hospitalists we must find with the intent to treat the scarlet letter of abnormal but accept the chronic unchangeable crimson that will show up on some diagnostic tests. We can only attempt to restore our patient to the baseline they had before and hope to prevent the next decompensation as best we can.
Saturday, October 8, 2011
I've been a professional student for (too) many years, but the education that I took for granted ended the day I started as attending. The dreaded morning report hosted by harried if dedicated clinicians, the complex grand rounds elucidated by leaders in medicine, noontime and core conferences in a multitude of subjects that were a constant time pressure in residency were rudely stolen the day I graduated. Within months of being a junior attending I was academically starved. Thus I started looking for other opportunities, seeking out the rounds I used to loath, traveling to conferences in far cities, and looking up events that just sounded interesting.
This week I attended the Illinois Transdisciplinary Obesity Prevention Program's (I-TOPP) Inaugural Biennial Symposium, which covered factors from the microscopic to the transnational of how obesity can be prevented in children. I'm an adult nocturnist, the youngest patient's I see are 19, and the only preventative medicine I do is of a more acute nature, as in preventing my patients from stopping oxygenating or perfusing. What's the point of going to something that I would be unlikely to have any "need" of. Knowledge isn't like that, it is insidious, flashes of brilliance (or snippets of insanity, depending on your point of view) occur while learning the most unlikely and seemingly unrelated things.
The symposium was opened by an epidemiologist at the Centers for Disease Control, Dr. Cynthia Ogden, who went through the data of childhood obesity and problems with the precision and accuracy of that data. Obesity in children is a huge problem, but may fortunately have plateaued. However those children are an added source of patients to an already growing cohort of obese older adults.
Obesity is often simplified as energy in (EIN) greater than energy out (EOUT), which to most clinicians, including myself, means eat fewer calories and expend more. However as I learned, this is a gross oversimplification, not of the equation, necessarily, but of the complex and multitudinous variables that contribute to both energy in and out, including (but certainly not limited to) calorie source, quantity, timing of consumption, genes, gut microbiota, being breastfed, psychosocial factors, location, economics, and many more. These variables are further defined by confusingly dependent and independent equations that have yet to be defined.
Genes! Impossible! Not according to Dr. Molly Bray, who examines genes in obesity. She told us about her and others research into genes that not only affect metabolism but behavior driving the obese to not only have decreased satiety but to shy away from exercise. Phenotypically these genes are environmentally dependent. In times of food scarcity they are genotypically pervasive but phenotypically absent, however when an "obesiogenic" environment presents itself, so too does the obesity phenotype.
One of the genes that has been discussed extensively is fat mass and obesity-associated protein (FTO). FTO encodes for proteins which can demethylate DNA, or promote gene products. This is an amazing concept, since dietary choices, if they are indeed choices and not mandated by genetic and environmental factors, produce concentration gradients of carbohydrates, lipids, and proteins which can interact directly with DNA, and therefore for may affect FTO and therefore drive demethylation. My conjecture is that this then in turn could produced a cascade effect on other genes involved in metabolism, cellular protein production, and behavior that would drive an organism toward obesity with different velocities. You are not only what you eat but you are regulated by it as well. It is as if the lumber and mortar got to to be the building supervisor as well.
The next invited speaker, Dr. Madeleine Sigman-Grant, discussed the development of the All 4 Kids Program, a community-based intervention in pre-schoolers to prevent obesity designed using a Logic Evaluation Model. I don't deal with preschoolers in a professional capacity nor am I planning any community interventions anytime soon. But it was a rewarding and interesting experience to see how someone worked through a Logic Evaluation Model to develop a preventative health intervention.
Dr. Stephen Matthews spoke on spatial polygamy, which is less risque than it sounds. The concept of spatial polygamy refers to individuals having multiple spatial interactions depending on the map technique used. Thus we are defined by zip codes, voting districts, census demographics, street addresses, telephone numbers, and e-mail addresses that redefine associations between individuals and their spatial or temporal dependence. Thus it is important to understand the source of our mapping data and the limits thereof.
This creates an interesting parallel in hospitalized patients. Their physical location in the hospital has little to do with their "therapeutic distance" from their physician. Therapeutic distance would be defined as the time between a patient having a need and it being taken care of. Two patients in the same room may have vastly different care demographics and therefore therapeutic distance, even if they are physically adjacent. The patient with the in-house hospitalist versus the traditional internist on-call from home may have significantly different response times to pages. The comanaged patient may or may not be more therapeutically isolated depending on how clear the nursing staff is on the division of duties between the physicians caring for the patient, i.e. if they don't know who to call, they will take longer to get the right physician to solve the problem.
Despite not being "my area" I certainly took a step outside my box, which would have expanded to include this new information, thus creating a new and larger box. Sometimes the box doesn't change but leaping outside the box in one area just places us within familiar and useful territory in another. Each day of our lives should be a leap outside of our old box, but within a new and larger box. The only way to achieve that is through the core competency of lifelong learning, that is no longer quite such a continuous feed after entering the post postgraduate world.
Sunday, October 2, 2011
A tongue in cheek application of the Laws of Thermodynamics as applied to medicine:
0th: If two diagnostic findings support a third, then they must support each other. No single diagnostic finding has ever made a diagnosis, it is a careful process of combining and comparing data that makes it possible to reach a diagnostic conclusion. Look at what your "facts" are, the diagnosis with the most "facts" supporting it is most likely the right one. Of course, facts in medicine are not as concrete as we would like to make them seem as demonstrated by false positive and negative results.
1st: You cannot win — A physician's diagnostic performance can be of one form (i.e. specific or sensitive) or another, but cannot be both. If you rule out a lot of different etiologies without ever ruling one in you are highly sensitive but not specific, and your patient still doesn't know what is wrong with them. If you always get positive results to your diagnostic inquiries you are highly specific but not very sensitive, and you are probably missing some disease in other patients because of missed testing.
2nd: You cannot break even — A negative diagnostic work-up does not decrease morbidity or mortality, while a positive one always increases both. Just because you didn't find a pathophysiological reason for a presentation doesn't mean that you didn't miss something or that your patient is any safer from future insults. Confirming a diagnosis simply means that you have named the disease and they now have the same increased risks as others with that disease as well as those from related or unrelated future insults.
3rd: You cannot leave the game — Absolutely false results must be worked-up, as there are no absolutes in medicine. Even the most spectacularly sound medical reasoning for explaining a false positive or random incidentaloma means nothing without further testing to corroborate that reasoning. Missed diagnoses kill, maim, and get doctors sued.