Penrose Box

Once we think outside the box, aren't we just inside a larger box? Once the ideas of one box leap outside, might we not be in another box?

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.

Laws of Thermodiagnostics

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.

Ten Eyes for Looking at Disease

Hypothesis: All disease is caused by some combination of

I Injury (caused by an exogenous agent, this would include hemorrhage)

I Inflammation (caused by the human organisms response to injury)

Y Immune (caused by under, over, or inappropriate response of the human self-defense mechanism)

I° Infection (caused by an exogenous microbial vector)

I Ischemia (caused by lack of blood flow)

i Inadequacy (caused by mechanical failure)

Aye Incompetence (caused by physiological failure, heart failure would presumably fall in both)

I Intoxication (caused by poison)

I Iatrogenic (caused by doctors)

¿ Idiopathic (caused by an unclear reason that is not included in the above, the cop-out)

When it is about the heart, it is all about relationships

Let us start our tale with little Ms. P who has a relationship with the broad shouldered Mr. QRS. In a normal stable relationship (NSR), Ms. P is always accompanied by Mr. QRS. They plan to go to weekly dance classes with some other partnered friends, but it's difficult with the sometimes early and other times late Sinus Arrhythmia. The Sinus Exit Block couple are always punctual when they make it, but sometimes skip a dance class or two with no warning, only to be there punctually next time. The hardest folks to do any planning with is the Sinus Arrest couple, they not only miss classes they never get the time right on the next one, arriving early or late.

Relationships can be challenging, like when Ms. P's ex-boyfriend Pac (Premature Atrial Contraction) drops in. He wants to hang out with P and reminisce about old times, messing up the lovebirds orderly schedule. The same thing happens when one of Mr. QRS' old frat brothers from the PVC (Premature Ventricular Contraction) house crashes their place for the weekend.

However relationships can also have more serious discord or blocks between them:

• A first degree block places some distance between the two lovers, but still they remain together.



• A second degree type I block is demonstrated by P and QRS Wenkebach who grow steadily further apart until QRS cheats and P dumps the bum, but she forgives him and takes him back only for the cycle to repeat.



• The more dastardly second degree type II occurs in the relationship between P and QRS Mobitz II, where despite the illusion of a stable relationship, QRS gets drunk, cheats, and they break up. P is still a forgiving lady and takes him back, but the scalawag QRS will do it again.



• Divorce, or the third degree block, has complete disassociation between P and QRS

The thin and rhythmless rapper A fib has so many ladies (his P's) that he is only erratically spotted. He is not to be confused with the equally anorexic hip hop artist A flutter who usually dates only twins and triplets. Neither one of these artists jams should be confused with the sudden vibrant beat of the techno SVT, he brings a rapid rhythm that looks almost sinus. Rumor has he too has an eating disorder. Everyone knows a player like their friend Mat (Multifocal Atrial Tachycardia), he's got a different P every week.

Not so for the amphetamine and steroid abusing loner V Tach, no Ps for him in his destructive quest. He used to be a founding member of the all male deathmetal band V Fib, but they were too chaotic even for him.

Four Rs of fluids

Resuscitation	Rehydration	Rectification	Regular (Maintenance)
Situation
Shock Decreased blood pressure Increased lactic acid Decreased urine output	Hypovolemia +/- electrolyte abnormalities "Pre-shock" (downtrends in blood pressure or urine output, increasing tachycardia) Diabetic ketoacidosis Rhabdomyolysis Post-obstructive diuresis Hypovolemic acute prerenal failure Pancreatitis	Electrolyte abnormalities +/- hypovolemia Hypovolemic hyponatremia Hypernatremia Hypokalemia Hyperchloremic acidosis	NPO
Choice of fluids
NS LR Albumin Hespan (but numerous contraindications)	Typically composition is directed by published guidelines (as in DKA) or fluids can be formulated by the considerations for maintenance fluids given in the column furthest to the right. Remember that 40 mEq of potassium in a peripheral line has a maximal infusion rate of 125 mL/hr	Hypovolemic hyponatremia 0.9% saline ("NS", 154 mEq Na/L) 3% saline (513 mEq Na/L) Hypernatremia 0.45% saline ("1/2 NS", 77 mEq Na/L) D5 (0 mEq Na/L) Hypokalemia Given normal renal function, assume 20 mEq of potassium increases serum potassium 0.25 mEq/L Hyperchloremic acidosis Assuming mild hyponatremia or normal sodium consider 150 mEq NaHCO3 in 1000 mL of D5 or free water (1)	Based on electrolytes, specifically: sodium, potassium, chloride, bicarbonate, and glucose (and occasionally phosphate) as well as blood pressure. If they are hypertensive consider hypotonic (1/2 NS) rather than isotonic (NS, LR) solutions even if they are mildly hyponatremic. If Na is within normal limits < 140 use NS, > 140 use 1/2 NS If K is within normal limits < 4 add 20 mEq KCl If hypoglycemic or marginally hyperglycemic use the D5 variant of the 1/2 NS or NS chosen above
Rate
20 mL/kg of crystalloid (NS or LR) over 15-20 minutes (thus a pressure bag is needed)	100-1000 mL/hr titrated to whatever volume deficit you are correcting	Hypovolemic hyponatremia The initial rate to correct by 10 mEq/L in 24 hours with NS is by rough calculation 1.35 x wgt [kg] for the rate in mL/hr. If using 3% saline multiply by 0.3 (2) Titrate the rate to serial BMP, if life threatening hyponatremia (e.g. seizures) correction may be more rapid for the first few hours but still < 10-12 mEq/L over 24 hours Hypernatremia The initial rate to correct by 10 mEq/L in 24 hours with D5 is by rough calculation 1.35 x wgt [kg] for the rate in mL/hr. If using 0.45% saline multiply by 2. Titrate the rate to serial BMP, such that the rate of correction < 10-12 mEq/L over 24 hours Hypokalemia Maximal correction via peripheral line is 40 mEq/L in 500 mL NS over four hours or 125 mL/hr Hyperchloremic acidosis As per "rehydration" rates	40-20-10 "rule" (for patients with normal electrolyte hemostatic mechanisms) 40 mL/hr for the first 10 kg 20 mL/hr for the second 10 kg 10 mL/hr for each additional 10 kg
How do you know it's working
Blood pressure increases Lactic acid decreases Urine output increases	Blood pressure, heart rate, and urine output improve ("preshock") Anion gap decreases (diabetic ketoacidosis) CK and renal function improve (rhabdomyolysis) Replace 50% of urine output per hour (post-obstructive diuresis) Urine output increases and renal function improves (hypovolemic acute prerenal failure) Amylase and lipase improve (pancreatitis)	Hypovolemic hyponatremia Sodium corrects by < 2 mEq/L every 4 hours, thus check BMP or I-STAT every 2-4 hours and titrate rate and composition of fluids appropriately Hypernatremia Sodium corrects by < 2 mEq/L every 4 hours, thus check BMP or I-STAT every 2-4 hours and titrate rate and composition of fluids appropriately Hypokalemia Electrolyte correction monitoring at most Q8H Hyperchloremic acidosis Electrolyte correction monitoring at most Q8H	The patient remains hemodynamically stable without electrolyte abnormalities or worsening renal function

1. Assuming NaHCO3 comes in a stock solution of 1 mEq/mL, then [C] = solute osmolarity / solution volume

   = solute osmolarity / (solute volume + solvent volume)

   = 150 mEq / (0.150 L + 1 L) = 130 mEq NaHCO3/L

   In 850 mL of solvent, then [C] = 150 / 1000 = 150 mEq Na HCO3/L

2. Assuming total body water [L] = 0.5 x wgt [kg] (acutally TBW fraction varies between 0.45 and 0.6 depending on gender and age). We want to change the current plasma sodium by 10 mEq/L/24 hours (i.e. the maximum safe change in serum sodium that will not precipitate central pontine myelinolysis) and recall that the concentration of sodium in 0.9% saline or NS is 154 mEq/L, then:

   infusion rate = 0.5 x wgt [kg] x 10 / 154 (L x mEq/L/24 hr) / (mEq/L)

   = 5 x 1000 x wgt [kg] / (154 x 24) mL/hr

   = 1.35 x wgt [kg] mL/hr for NS

   If we are using 3% saline, multiply by 0.9/3 (0.9% / 3%) or 0.3

   In the case of hypernatremia, we know that 1/2 NS is half the concentration of NS, such that if we did a similar infusion rate calculation the denominator would be half what is above, or simply multiplying by 2.

Encephalopathy in a nutshell

Although not the definitive, all encompassing, reasons for encephalopathy/delirium/altered mental status, this short list certainly covers many of the most prevalent causes.

Etiology	Physical Exam	Bedside Diagnostic Tests	History	STAT Diagnostic Tests
"Bugs" Infection	Temperature SpO2 Meningeal signs Lines (vascular, GI, GU)		Headache Aspiration Productive cough Vomiting / Diarrhea Urinary changes	CXR UA and urine c/s Blood c/s Sputum c/s C. difficile toxin
"Drugs" Side effects of and withdrawal from drugs		Naloxone trial	MAR (narcotics, corticosteroids, CNS agents) Review home medications Alcohol/substance abuse
"Lytes" Electrolyte abnormalities particularly hypo- and hyperosmolar states		I-STAT	Ins/Outs	BMP Serum osmolarity
"Plights" Inadequate pain control	Pain scale Abdominal examination	Bladder scan
"Beating" Cardiac arrhythmia and ischemia	Heart rate Blood pressure Jugular venous pulsation Heart murmurs and additional sounds	Telemetry I-STAT Troponin		EKG Cardiac markers BNP
"Bleeding" Acute blood loss	Scleral pallor Rectal exam	Fecal occult blood test I-STAT (ABG also has an H&H)	Recent surgery Anticoagulation	CBC
"Gases" Hypoxemia or hypercarbia Acidosis or alkalosis	Respiratory rate SpO2	ABG	History of hypercarbia Previous ABG
"Glucose" Hypo- and hyperglycemia		Accu-check I-STAT	Diabetes mellitus Insulin or oral antihyperglycemic medications
"Gourd" Intracranial pathology (i.e. stroke, mass effect, traumatic brain injury) Seizure	Neurological examination		Documentation of seizure-like activity without formal history of seizure Trauma History of dementia or seizure	CT head without contrast

CDC Warns of Zombiepocalypse